subject:(Epithelial cells)

University of Hong Kong

1. 周伊润; Zhou, Yirun. The anti-oxidant potential of different flavonoids in human bronchial epithelial cells.

Degree: Master of Medical Sciences, 2015, University of Hong Kong

URL: Zhou, Y. [周伊润]. (2015). The anti-oxidant potential of different flavonoids in human bronchial epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659899 ; http://hdl.handle.net/10722/221520

► Oxidative stress is known to play a pathogenetic role in neurodegenerative, cardiovascular, lung and liver diseases. It increases as a result of an imbalance between… (more)

▼ Oxidative stress is known to play a pathogenetic role in neurodegenerative, cardiovascular, lung and liver diseases. It increases as a result of an imbalance between the production of oxidants and the activity of the antioxidant defense system. The antioxidants and free radical scavengers eliminate the excessive reactive oxygen species, prevent their formation and promote the activity of endogenous anti-oxidant mechanism. Flavonoids are well-known to possess anti-oxidant properties. In the present study, the anti-oxidant potentials of different flavonoids from different sub-families were examined in airway epithelial cells. Moreover, experiments were designed to examine whether or not flavonoids reduce the oxidative stress in the airway epithelium due to bacterial infection, and if so, whether or not they produce the effects by activating the two major endogenous anti-oxidant systems, catalase and glutathione. Human bronchial epithelial BEAS-2B cells were treated with different flavonoids in the absence and presence of the bacterial endotoxin, lipopolysaccharides (LPS). The concentration of 8-isoprostane, a biomarker for oxidative stress, in the culture medium was measured, as an indication of the antioxidant potentials of the flavonoids. The activity of catalase and the cellular level of glutathione in BEAS-2B cells after the treatments were also evaluated. Among the 17 flavonoids tested, pelargonidin was the only flavonoid that could reduce 8-isoprostane levels in conditions with and without LPS. Quercetin showed an anti-oxidant effect only in cells without LPS treatment while phloretin reduced 8-isoprostane level only in cells treated with LPS. Daidzein was found to have a pro-oxidant effect in the presence of LPS. Unexpectedly, quercetin reduced catalase activity in BEAS-2B cells not treated with LPS, and had no effect on the cellular glutathione level. Daidzein did not affect catalase activity and glutathione level, similarly to catechin[which served as the “negative control” for flavonoids in the study(as it did not affect the 8-isoprostane level in conditions with and without LPS)]. In conclusion, not all flavonoids produce anti-oxidant effects in human bronchial epithelial cells; only quercetin, pelargonidin and phloretin appear to offer anti-oxidative protection. However, quercetin inhibits catalase in BEAS-2B cells without LPS treatment, thus suggesting a possible pro-oxidant action under basal conditions. Therefore, cautions should be taken in considering the use of quercetin as a health supplement against cellular oxidative stress. Similarly, the observation that daidzein may have pro-oxidant effects in conditions with LPS also poses a warning for the use of this flavonoid as a health supplement. The proposal that flavonoids have pro-oxidant effects appears contradictive with their reported effects in some other studies; the discrepancy may be explained by the differences in the cell types, the biomarker and the concentration of flavonoid used. Therefore, the present findings prompt the need for a…

Subjects/Keywords: Epithelial cells; Flavonoids

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APA (6^th Edition):

周伊润; Zhou, Y. (2015). The anti-oxidant potential of different flavonoids in human bronchial epithelial cells. (Masters Thesis). University of Hong Kong. Retrieved from Zhou, Y. [周伊润]. (2015). The anti-oxidant potential of different flavonoids in human bronchial epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659899 ; http://hdl.handle.net/10722/221520

Chicago Manual of Style (16^th Edition):

周伊润; Zhou, Yirun. “The anti-oxidant potential of different flavonoids in human bronchial epithelial cells.” 2015. Masters Thesis, University of Hong Kong. Accessed September 15, 2019. Zhou, Y. [周伊润]. (2015). The anti-oxidant potential of different flavonoids in human bronchial epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659899 ; http://hdl.handle.net/10722/221520.

MLA Handbook (7^th Edition):

周伊润; Zhou, Yirun. “The anti-oxidant potential of different flavonoids in human bronchial epithelial cells.” 2015. Web. 15 Sep 2019.

Vancouver:

周伊润; Zhou Y. The anti-oxidant potential of different flavonoids in human bronchial epithelial cells. [Internet] [Masters thesis]. University of Hong Kong; 2015. [cited 2019 Sep 15]. Available from: Zhou, Y. [周伊润]. (2015). The anti-oxidant potential of different flavonoids in human bronchial epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659899 ; http://hdl.handle.net/10722/221520.

Council of Science Editors:

周伊润; Zhou Y. The anti-oxidant potential of different flavonoids in human bronchial epithelial cells. [Masters Thesis]. University of Hong Kong; 2015. Available from: Zhou, Y. [周伊润]. (2015). The anti-oxidant potential of different flavonoids in human bronchial epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5659899 ; http://hdl.handle.net/10722/221520

University of Hong Kong

2. Liu, Mengfei. Epithelial morphogenesis in three-dimensional cell culture system.

Degree: PhD, 2014, University of Hong Kong

URL: Liu, M. [刘梦菲]. (2014). Epithelial morphogenesis in three-dimensional cell culture system. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387985 ; http://dx.doi.org/10.5353/th_b5387985 ; http://hdl.handle.net/10722/208611

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In human body, the most common structures formed by epithelial cells are hollow cysts or tubules. The key feature of the cysts and tubules is… (more)

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In human body, the most common structures formed by epithelial cells are hollow cysts or tubules. The key feature of the cysts and tubules is the central lumen, which is lined by epithelial cell sheets. The central lumen allows material exchange, thus it is indispensable for the proper function of the epithelial tissue. In order to understand the way that the epithelial cells form highly specialized structure, an in vitro three-dimensional (3D) culture system was established. The Caco-2 cells were embedded in reconstituted basement membrane termed matrigel, whose biochemical constitution and physical properties were similar with the in vivo environment. The Caco-2 cells in matrigel spontaneously formed spherical multi-cell cysts, which could continuously expand. The confocal imaging and reconstruction technique helped understand the cyst structure and its formation process. The cysts developed central lumen surrounded by a layer of polarized cells. The apical domain of the cells faced the lumen, while the basal domain attached to the extracellular matrix. In the mature cysts, fluid was secreted by the cells around the lumen at the apical domain, and accumulated in the central lumen. The laser burning experiment showed that the intraluminal pressure was higher than the outer environment. The intact cell sheet was required to keep the engorged morphology of the cysts. The tension of the cell layer balanced with the intraluminal pressure. To investigate the effect of pressure on cyst development, the cysts were treated with cholera toxin, which could increase intraluminal pressure through promoting apical secretion. The time-lapse images showed that under cholera toxin treatment, the expansion of the cysts was accelerated. The high intraluminal pressure led to shape change of thecells, followed by increase in cell proliferation rate. Cholera toxin itself could not promote cell growth. In the3D cultured cysts, it was the increased intraluminal pressure that directly induced the acceleration of cell proliferation. It indicated that not only biochemical signals, but also mechanical force, contributed to epithelial morphogenesis. The mechanical stimulation could be converted into biochemical signals, further affect cell behavior. In response to mechanical stimulation, the focal adhesion kinase was activated in the cells around the cyst lumen. Furthermore, the microarray analysis suggested that multiple signaling pathways were altered under intraluminal pressure stimulation, including the pathways related to cytoskeleton organization, cell cycle and cell adhesion. Taken together, comparing with the conventional two-dimensional cell culture on rigid surface, the three-dimensional culture system provided the cells a more physiological environment. The 3D culture system allows the epithelial cells to form well-organized hollow structure. It is a convenient model for investigating the process and mechanism of epithelial morphogenesis.

published_or_final_version

Biochemistry

Doctoral

Doctor of Philosophy

Subjects/Keywords: Epithelial cells; Human cell culture

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APA (6^th Edition):

Liu, M. (2014). Epithelial morphogenesis in three-dimensional cell culture system. (Doctoral Dissertation). University of Hong Kong. Retrieved from Liu, M. [刘梦菲]. (2014). Epithelial morphogenesis in three-dimensional cell culture system. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387985 ; http://dx.doi.org/10.5353/th_b5387985 ; http://hdl.handle.net/10722/208611

Chicago Manual of Style (16^th Edition):

Liu, Mengfei. “Epithelial morphogenesis in three-dimensional cell culture system.” 2014. Doctoral Dissertation, University of Hong Kong. Accessed September 15, 2019. Liu, M. [刘梦菲]. (2014). Epithelial morphogenesis in three-dimensional cell culture system. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387985 ; http://dx.doi.org/10.5353/th_b5387985 ; http://hdl.handle.net/10722/208611.

MLA Handbook (7^th Edition):

Liu, Mengfei. “Epithelial morphogenesis in three-dimensional cell culture system.” 2014. Web. 15 Sep 2019.

Vancouver:

Liu M. Epithelial morphogenesis in three-dimensional cell culture system. [Internet] [Doctoral dissertation]. University of Hong Kong; 2014. [cited 2019 Sep 15]. Available from: Liu, M. [刘梦菲]. (2014). Epithelial morphogenesis in three-dimensional cell culture system. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387985 ; http://dx.doi.org/10.5353/th_b5387985 ; http://hdl.handle.net/10722/208611.

Council of Science Editors:

Liu M. Epithelial morphogenesis in three-dimensional cell culture system. [Doctoral Dissertation]. University of Hong Kong; 2014. Available from: Liu, M. [刘梦菲]. (2014). Epithelial morphogenesis in three-dimensional cell culture system. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5387985 ; http://dx.doi.org/10.5353/th_b5387985 ; http://hdl.handle.net/10722/208611

University of Hong Kong

3. Ling, Ka-ho. Polyphenol-mediated protective effects against bacterial translocation across intestinal epithelial cells and their mechanisms.

Degree: PhD, 2015, University of Hong Kong

URL: Ling, K. [凌加豪]. (2015). Polyphenol-mediated protective effects against bacterial translocation across intestinal epithelial cells and their mechanisms. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5699899. ; http://dx.doi.org/10.5353/th_b5699899 ; http://hdl.handle.net/10722/236746

► An intact intestinal barrier maintains gut health by keeping pathogens at bay. Normally, the intestinal barrier is very effective —the luminal side is heavily infested… (more)

▼ An intact intestinal barrier maintains gut health by keeping pathogens at bay. Normally, the intestinal barrier is very effective —the luminal side is heavily infested with more than 1012microbes per milliliter of fecal materials, yet the basolateral side (portal blood and mesenteric lymph nodes) is virtually sterile. However, insults from the external environment, such as food toxins, drugs and pathogens, can undermine intestinal integrity. A compromised intestinal barrier (leaky gut) is prone to bacterial translocation, predisposing one to various gastrointestinal disorders. Polyphenols (PPs) are widely present in plant-based foods and beverages, with daily human consumption estimated at up to several hundred milligrams. Therefore, intestinal epithelial cells (IECs) are constantly and directly exposed to a high dose of PPs. However, the effect of PPs on the intestinal barrier remains largely unexplored. The present study aimed to identify dietary PPs that can improve gut health by reducing bacterial translocation across IEC monolayers. Principal action mechanism(s) were characterized. Cell-based in vitroassays were performed using polarized porcine IECs, IPEC-J2, cultured on permeable membrane supports. Translocation of Escherichia coliacross the cell monolayers was first determined by agar plate counting. Further mechanistic analyses —applying electrophysiology assay, unidirectional tracer flux assay, antibacterial assay, quantitative reverse transcriptase polymerase chain reaction, protein immunoblotting, enzyme-linked immunosorbent assay, and Luminex multiplex assay —were then undertaken to characterize PP-mediated protective effects in normal and deoxynivalenol (DON)-damaged cell monolayers. Selected dietary PPs, including chlorogenic acid, epigallocatechin gallate (EGCG), quercetin, resveratrol (RES) and rutin, were screened. It was revealed that EGCG and RES, present in green tea and red wine respectively, significantly reduced E. colitranslocation. In further mechanistic investigation, the two PPs were shown to function differently: RES enhanced the physical barrier (strengthening tight junctions), while EGCG enhanced the immunological barrier (inducing antimicrobial peptides secretion). In detail, RES promoted the assembly of claudin-4 to the tight junction complex in normal cells, and protected against DON-induced barrier dysfunction by preventing dissociation of claudin-4 from actin cytoskeleton, through modulation of IL-6 and IL-8 secretion in a mitogen activated protein kinase (MAPK)-dependent response. Meanwhile, EGCG reduced bacterial translocation, in normal and DON-damaged cells, by stimulating the release of cytoplasmic β-defensin-1 via a MAPK-independent pathway, as well as upregulating gene expression and production ofβ-defensin-2 via a p38 MAPK signaling pathway. The present study reveals, for the first time, that PPs can reduce bacterial translocation across IECs. Our findings have highlighted a great potential of dietary intervention with PPs to uphold intestinal…

Subjects/Keywords: Epithelial cells; Polyphenols; Intestines - Microbiology

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APA (6^th Edition):

Ling, K. (2015). Polyphenol-mediated protective effects against bacterial translocation across intestinal epithelial cells and their mechanisms. (Doctoral Dissertation). University of Hong Kong. Retrieved from Ling, K. [凌加豪]. (2015). Polyphenol-mediated protective effects against bacterial translocation across intestinal epithelial cells and their mechanisms. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5699899. ; http://dx.doi.org/10.5353/th_b5699899 ; http://hdl.handle.net/10722/236746

Chicago Manual of Style (16^th Edition):

Ling, Ka-ho. “Polyphenol-mediated protective effects against bacterial translocation across intestinal epithelial cells and their mechanisms.” 2015. Doctoral Dissertation, University of Hong Kong. Accessed September 15, 2019. Ling, K. [凌加豪]. (2015). Polyphenol-mediated protective effects against bacterial translocation across intestinal epithelial cells and their mechanisms. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5699899. ; http://dx.doi.org/10.5353/th_b5699899 ; http://hdl.handle.net/10722/236746.

MLA Handbook (7^th Edition):

Ling, Ka-ho. “Polyphenol-mediated protective effects against bacterial translocation across intestinal epithelial cells and their mechanisms.” 2015. Web. 15 Sep 2019.

Vancouver:

Ling K. Polyphenol-mediated protective effects against bacterial translocation across intestinal epithelial cells and their mechanisms. [Internet] [Doctoral dissertation]. University of Hong Kong; 2015. [cited 2019 Sep 15]. Available from: Ling, K. [凌加豪]. (2015). Polyphenol-mediated protective effects against bacterial translocation across intestinal epithelial cells and their mechanisms. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5699899. ; http://dx.doi.org/10.5353/th_b5699899 ; http://hdl.handle.net/10722/236746.

Council of Science Editors:

Ling K. Polyphenol-mediated protective effects against bacterial translocation across intestinal epithelial cells and their mechanisms. [Doctoral Dissertation]. University of Hong Kong; 2015. Available from: Ling, K. [凌加豪]. (2015). Polyphenol-mediated protective effects against bacterial translocation across intestinal epithelial cells and their mechanisms. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5699899. ; http://dx.doi.org/10.5353/th_b5699899 ; http://hdl.handle.net/10722/236746

University of Hong Kong

4. 周嫄; Zhou, Yuan. Dynamics of Epstein-Barr virus episomes in infected epithelial cells.

Degree: PhD, 2016, University of Hong Kong

URL: Zhou, Y. [周嫄]. (2016). Dynamics of Epstein-Barr virus episomes in infected epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5784851. ; http://dx.doi.org/10.5353/th_b5784851 ; http://hdl.handle.net/10722/240587

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Epstein-Barr virus (EBV) is the first identified human tumor virus. It readily infects human memory B cells and establishes life-long latency after primary infection. EBV… (more)

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Epstein-Barr virus (EBV) is the first identified human tumor virus. It readily infects human memory B cells and establishes life-long latency after primary infection. EBV infection is also associated with specific types of carcinomas with lymphoepithelioma properties, including the undifferentiated nasopharyngeal carcinoma and EBV-associated gastric adenocarcinoma. EBV genomes are found in almost all of these cancer cells. However, how the EBV genomes persist in the proliferating host cells is poorly understood. The replication of EBV genomes in each cell cycle and their partitioning to daughter cells are believed to be crucial for the persistence of EBV in host cells. Previous studies have either investigated the replication and partition of EBV in live cells using EBV-derived plasmids which contained partial EBV genome or through detection of EBV episomes by FISH in fixed cells. The replication and partition of the whole EBV episomes in live cells have never been examined. In the present study, the dynamics of the replication and segregation of the whole EBV episomes during latent infection in live epithelial cells was examined for the first time. A newly engineered visible EBV was used in the study. The dynamics of replication and partitioning of visible EBV genomes were characterized at single cell level. Interestingly, unlicensed replication of EBV genomes (EBV replicated more than once per cell cyle) was observed for the first time in 13.6% of the infected cells. Licensed replication of EBV (EBV replicated once per cell cycle) was observed in 63.6% of cells, and no-replication of EBV (no EBV replication per cell cycle) was observed in 22.7% of cells. On average, EBV genomes replicated to 1.61 folds per cell cycle per cell. In addition, the EBV episomes preferred to localize at host nuclear regions active for replication and transcriptions. Lastly, EBV episomes from mother cells partitioned unequally into daughter cells. The unlicensed replication and unequal partitioning of EBV episomes may compensate for the imperfect replication, giving rise to a wide range of distribution of EBV copy per cell within a clonal population. The present study characterized the dynamics of EBV replication and partitioning in epithelial cells during latent infection at single cell level. This study also contributed to the mechanism for EBV maintenance in epithelial cells. The establishment of latent infection of visible EBV in epithelial cells and the imaging-analysis system developed in this study can be applied to future investigation of virus-host interaction to further our understanding of the role of EBV in the pathogenesis of the EBV-associated carcinoma.

published_or_final_version

Biomedical Sciences

Doctoral

Doctor of Philosophy

Subjects/Keywords: Epstein-Barr virus; Epithelial cells

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

周嫄; Zhou, Y. (2016). Dynamics of Epstein-Barr virus episomes in infected epithelial cells. (Doctoral Dissertation). University of Hong Kong. Retrieved from Zhou, Y. [周嫄]. (2016). Dynamics of Epstein-Barr virus episomes in infected epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5784851. ; http://dx.doi.org/10.5353/th_b5784851 ; http://hdl.handle.net/10722/240587

Chicago Manual of Style (16^th Edition):

周嫄; Zhou, Yuan. “Dynamics of Epstein-Barr virus episomes in infected epithelial cells.” 2016. Doctoral Dissertation, University of Hong Kong. Accessed September 15, 2019. Zhou, Y. [周嫄]. (2016). Dynamics of Epstein-Barr virus episomes in infected epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5784851. ; http://dx.doi.org/10.5353/th_b5784851 ; http://hdl.handle.net/10722/240587.

MLA Handbook (7^th Edition):

周嫄; Zhou, Yuan. “Dynamics of Epstein-Barr virus episomes in infected epithelial cells.” 2016. Web. 15 Sep 2019.

Vancouver:

周嫄; Zhou Y. Dynamics of Epstein-Barr virus episomes in infected epithelial cells. [Internet] [Doctoral dissertation]. University of Hong Kong; 2016. [cited 2019 Sep 15]. Available from: Zhou, Y. [周嫄]. (2016). Dynamics of Epstein-Barr virus episomes in infected epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5784851. ; http://dx.doi.org/10.5353/th_b5784851 ; http://hdl.handle.net/10722/240587.

Council of Science Editors:

周嫄; Zhou Y. Dynamics of Epstein-Barr virus episomes in infected epithelial cells. [Doctoral Dissertation]. University of Hong Kong; 2016. Available from: Zhou, Y. [周嫄]. (2016). Dynamics of Epstein-Barr virus episomes in infected epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5784851. ; http://dx.doi.org/10.5353/th_b5784851 ; http://hdl.handle.net/10722/240587

University of Hong Kong

5. Lai, Wing-yin, Joan. The effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells.

Degree: Master of Medical Sciences, 2013, University of Hong Kong

URL: Lai, W. J. [賴穎賢]. (2013). The effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5091422 ; http://dx.doi.org/10.5353/th_b5091422 ; http://hdl.handle.net/10722/193537

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Chronic obstructive pulmonary disease (COPD) is a highly prevalent disease in the elderly. It is currently the fourth leading cause of death and will become… (more)

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Chronic obstructive pulmonary disease (COPD) is a highly prevalent disease in the elderly. It is currently the fourth leading cause of death and will become the third by 2030. Cigarette smoke is the major cause of COPD pathogenesis, resulting from the burden of oxidants, which stimulates the production of inflammatory chemokines, leading to the influx of inflammatory cells into the airways and causing chronic inflammation. Due to lung infection by bacteria, such as Pseudomonas Aeruginosa during acute exacerbation in COPD, cigarette smoking might induce an immunosuppressive effect, which leads to bacteria colonization in the airways and further contributes to the chronic inflammation in the airway of COPD. Furthermore, cigarette smoke-induced production of reactive oxygen species (ROS) also plays an important role in the pathogenesis of COPD, however, N-acetyl-L-cysteine (NAC), which has been administered for the treatment of COPD as a mucolytic agent, also showed antioxidant and anti-inflammatory effect. The exact mechanism or cellular pathway through which cigarette smoke suppresses bacteria-induced inflammatory response and how NAC acts as an anti-inflammatory agent still remains uncertain. This study aims to investigate the effect of cigarette smoke and lipopolysaccharide (LPS) alone or in combination on the release of pro-inflammatory chemokines and to elucidate cigarette smoke-induced chemokines release in the presence and absence of NAC. Both cigarette smoke and LPS alone induced the release of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1).Cigarette smoke suppressed the LPS-induced IL-8 and MCP-1release. NAC reduced both basal and cigarette smoke-induced secretion of these inflammatory chemokines. Moreover, Western blot demonstrated that cigarette smoke activated AMPKα phosphorylation, which was suppressed with NAC pretreatment, suggesting that NAC might have inhibitory effect on the release of chemokine release via the AMPK pathway. Our current data suggests that there may be a link between ROS generation to AMPK activation and chemokine release in BEAS-2B cells.

published_or_final_version

Pharmacology and Pharmacy

Master

Master of Medical Sciences

Subjects/Keywords: Epithelial cells; Cigarette smoke; Endotoxins

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APA (6^th Edition):

Lai, Wing-yin, J. (2013). The effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells. (Masters Thesis). University of Hong Kong. Retrieved from Lai, W. J. [賴穎賢]. (2013). The effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5091422 ; http://dx.doi.org/10.5353/th_b5091422 ; http://hdl.handle.net/10722/193537

Chicago Manual of Style (16^th Edition):

Lai, Wing-yin, Joan. “The effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells.” 2013. Masters Thesis, University of Hong Kong. Accessed September 15, 2019. Lai, W. J. [賴穎賢]. (2013). The effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5091422 ; http://dx.doi.org/10.5353/th_b5091422 ; http://hdl.handle.net/10722/193537.

MLA Handbook (7^th Edition):

Lai, Wing-yin, Joan. “The effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells.” 2013. Web. 15 Sep 2019.

Vancouver:

Lai, Wing-yin J. The effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells. [Internet] [Masters thesis]. University of Hong Kong; 2013. [cited 2019 Sep 15]. Available from: Lai, W. J. [賴穎賢]. (2013). The effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5091422 ; http://dx.doi.org/10.5353/th_b5091422 ; http://hdl.handle.net/10722/193537.

Council of Science Editors:

Lai, Wing-yin J. The effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells. [Masters Thesis]. University of Hong Kong; 2013. Available from: Lai, W. J. [賴穎賢]. (2013). The effects of cigarette smoke on lipopolysaccharide-mediated responses in airway epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5091422 ; http://dx.doi.org/10.5353/th_b5091422 ; http://hdl.handle.net/10722/193537

University of Hong Kong

6. Nian, Shen. In vitro and in vivo evaluation of iris pigment epithelial cells cultured on surface modified expanded-polytetrafluorethylene substrates as a potential therapeutic strategy for retinal degeneration.

Degree: PhD, 2013, University of Hong Kong

URL: Nian, S. [年申]. (2013). In vitro and in vivo evaluation of iris pigment epithelial cells cultured on surface modified expanded-polytetrafluorethylene substrates as a potential therapeutic strategy for retinal degeneration. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4979921 ; http://dx.doi.org/10.5353/th_b4979921 ; http://hdl.handle.net/10722/193403

► Retinal degenerative diseases are diseases that may severely affect vision of people at different ages. These include retinitis pigmentosa (RP) and age-related macular degeneration (AMD).… (more)

▼ Retinal degenerative diseases are diseases that may severely affect vision of people at different ages. These include retinitis pigmentosa (RP) and age-related macular degeneration (AMD). The current treatments for these diseases are limited. Since dysfunction and atrophy of the RPE are the key factors in the development of retinal degenerative diseases, transplantation of healthy retinal pigment epithelial (RPE) cells might be a promising therapeutic strategy. However, homologous RPE cells may lead to host immune rejection and harvesting autologous RPE cells may cause severe complications. Autologous iris pigment epithelial (IPE) cells, which are relatively easy to obtain, possess the same embryonic origin and share similar characteristics as RPE cells. Therefore, they may be used as a substitute of RPE cells for transplantation. Increasing interests have been demonstrated with the use of substrate to support cell attachment, proliferation and differentiation, so that transplanted cells could maintain the differentiated phenotype and perform their normal functions. However, degradation of biodegradable substrates may cause the breakdown of functional cell monolayer and produce toxic byproducts. Therefore, the aim of current study is to investigate the in vitro characteristics of rat IPE cells cultured on surface modified non-degradable expanded-polytetrafluorethylene (ePTFE) substrates and host response to the substrates without cells. Primary pure IPE cells were successfully isolated from rat eyes, which provided abundant cells for subsequent experiments. IPE cells harvested from both Long Evans rats and Dark Agouti rats proliferated and reached confluence on fibronectin coated n-heptylamine modified (F-HA) ePTFE substrates. These cells exhibited cuboidal or polygonal morphology with heavy pigmentation. In addition to the typical epithelial cell morphology, rat IPE cells grown on F-HA ePTFE substrates were able to form a cell monolayer with functional formation of tight junctional complex between neighboring cells. The IPE cell monolayers also demonstrated increased phagocytosis of photoreceptor outer segments (POS) with time and expression of cellular retinylaldehyde-binding protein (CRALBP) that served an important role in the conversion of all-trans-retinal to 11-cis-retinal in visual cycle. In the in vivo study, F-HA ePTFE substrate was successfully transplanted into the subretinal space of Royal College of Surgeons (RCS) rat, which is a well-recognized animal model of retinal degeneration. The F-HA ePTFE substrate remained flat up to 4 weeks after transplantation and did not induce significant up-regulation of pro-inflammatory cytokines TNFα and IL1β as well as activation of Müller cells and astrocytes which occurred in response to retinal inflammation. In conclusion, rat IPE cells that were grown on F-HA ePTFE substrate were able to establish a monolayer with functional tight junctions and RPE-specific functions. The F-HA ePTFE substrate demonstrated good biocompatibility in the subretinal space of RCS…

Subjects/Keywords: Retinal degeneration - Treatment; Epithelial cells

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APA (6^th Edition):

Nian, S. (2013). In vitro and in vivo evaluation of iris pigment epithelial cells cultured on surface modified expanded-polytetrafluorethylene substrates as a potential therapeutic strategy for retinal degeneration. (Doctoral Dissertation). University of Hong Kong. Retrieved from Nian, S. [年申]. (2013). In vitro and in vivo evaluation of iris pigment epithelial cells cultured on surface modified expanded-polytetrafluorethylene substrates as a potential therapeutic strategy for retinal degeneration. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4979921 ; http://dx.doi.org/10.5353/th_b4979921 ; http://hdl.handle.net/10722/193403

Chicago Manual of Style (16^th Edition):

Nian, Shen. “In vitro and in vivo evaluation of iris pigment epithelial cells cultured on surface modified expanded-polytetrafluorethylene substrates as a potential therapeutic strategy for retinal degeneration.” 2013. Doctoral Dissertation, University of Hong Kong. Accessed September 15, 2019. Nian, S. [年申]. (2013). In vitro and in vivo evaluation of iris pigment epithelial cells cultured on surface modified expanded-polytetrafluorethylene substrates as a potential therapeutic strategy for retinal degeneration. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4979921 ; http://dx.doi.org/10.5353/th_b4979921 ; http://hdl.handle.net/10722/193403.

MLA Handbook (7^th Edition):

Nian, Shen. “In vitro and in vivo evaluation of iris pigment epithelial cells cultured on surface modified expanded-polytetrafluorethylene substrates as a potential therapeutic strategy for retinal degeneration.” 2013. Web. 15 Sep 2019.

Vancouver:

Nian S. In vitro and in vivo evaluation of iris pigment epithelial cells cultured on surface modified expanded-polytetrafluorethylene substrates as a potential therapeutic strategy for retinal degeneration. [Internet] [Doctoral dissertation]. University of Hong Kong; 2013. [cited 2019 Sep 15]. Available from: Nian, S. [年申]. (2013). In vitro and in vivo evaluation of iris pigment epithelial cells cultured on surface modified expanded-polytetrafluorethylene substrates as a potential therapeutic strategy for retinal degeneration. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4979921 ; http://dx.doi.org/10.5353/th_b4979921 ; http://hdl.handle.net/10722/193403.

Council of Science Editors:

Nian S. In vitro and in vivo evaluation of iris pigment epithelial cells cultured on surface modified expanded-polytetrafluorethylene substrates as a potential therapeutic strategy for retinal degeneration. [Doctoral Dissertation]. University of Hong Kong; 2013. Available from: Nian, S. [年申]. (2013). In vitro and in vivo evaluation of iris pigment epithelial cells cultured on surface modified expanded-polytetrafluorethylene substrates as a potential therapeutic strategy for retinal degeneration. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4979921 ; http://dx.doi.org/10.5353/th_b4979921 ; http://hdl.handle.net/10722/193403

University of California – Merced

7. Pettengill, Matthew Aaron. Danger signals and the regulation of Chlamydia infection in epithelial cells.

Degree: Quantitative and Systems Biology, 2010, University of California – Merced

URL: http://www.escholarship.org/uc/item/3w77g2qc

► Bacterial infections of the mucosal epithelium initiate inflammation of the local tissues, which leads to changes in the molecular profile of the extracellular milieu, including… (more)

Subjects/Keywords: Biology.; Chlamydia.; Epithelial cells.

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APA (6^th Edition):

Pettengill, M. A. (2010). Danger signals and the regulation of Chlamydia infection in epithelial cells. (Thesis). University of California – Merced. Retrieved from http://www.escholarship.org/uc/item/3w77g2qc

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Pettengill, Matthew Aaron. “Danger signals and the regulation of Chlamydia infection in epithelial cells.” 2010. Thesis, University of California – Merced. Accessed September 15, 2019. http://www.escholarship.org/uc/item/3w77g2qc.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Pettengill, Matthew Aaron. “Danger signals and the regulation of Chlamydia infection in epithelial cells.” 2010. Web. 15 Sep 2019.

Vancouver:

Pettengill MA. Danger signals and the regulation of Chlamydia infection in epithelial cells. [Internet] [Thesis]. University of California – Merced; 2010. [cited 2019 Sep 15]. Available from: http://www.escholarship.org/uc/item/3w77g2qc.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Pettengill MA. Danger signals and the regulation of Chlamydia infection in epithelial cells. [Thesis]. University of California – Merced; 2010. Available from: http://www.escholarship.org/uc/item/3w77g2qc

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

McGill University

8. MacLeod, R. John. Signal Transduction of Volume Regulation in Villus Epithelial Cells.

Degree: PhD, Department of Medicine, Division of Experimental Medicine, 1996, McGill University

URL: http://digitool.library.mcgill.ca/thesisfile157015.pdf

►

Note:

Volume increases of any magnitude in Na+ -absorbing jejunal epithelial cells result in the activation of K+ and et· channels; the resultant é and… (more)

Subjects/Keywords: Epithelial cells

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APA (6^th Edition):

MacLeod, R. J. (1996). Signal Transduction of Volume Regulation in Villus Epithelial Cells. (Doctoral Dissertation). McGill University. Retrieved from http://digitool.library.mcgill.ca/thesisfile157015.pdf

Chicago Manual of Style (16^th Edition):

MacLeod, R John. “Signal Transduction of Volume Regulation in Villus Epithelial Cells.” 1996. Doctoral Dissertation, McGill University. Accessed September 15, 2019. http://digitool.library.mcgill.ca/thesisfile157015.pdf.

MLA Handbook (7^th Edition):

MacLeod, R John. “Signal Transduction of Volume Regulation in Villus Epithelial Cells.” 1996. Web. 15 Sep 2019.

Vancouver:

MacLeod RJ. Signal Transduction of Volume Regulation in Villus Epithelial Cells. [Internet] [Doctoral dissertation]. McGill University; 1996. [cited 2019 Sep 15]. Available from: http://digitool.library.mcgill.ca/thesisfile157015.pdf.

Council of Science Editors:

MacLeod RJ. Signal Transduction of Volume Regulation in Villus Epithelial Cells. [Doctoral Dissertation]. McGill University; 1996. Available from: http://digitool.library.mcgill.ca/thesisfile157015.pdf

University of North Carolina – Greensboro

9. Covell, Alan D. At the interface: biotic-abiotic interactions between substrates and a model epithelium.

Degree: 2015, University of North Carolina – Greensboro

URL: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=18887

► The need for determining the fundamental mechanisms that define the interaction of biological systems with underlying materials, both natural and synthetic, is important as humanity… (more)

Subjects/Keywords: Epithelial cells; Cell interaction; Nanotechnology

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APA (6^th Edition):

Covell, A. D. (2015). At the interface: biotic-abiotic interactions between substrates and a model epithelium. (Doctoral Dissertation). University of North Carolina – Greensboro. Retrieved from http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=18887

Chicago Manual of Style (16^th Edition):

Covell, Alan D. “At the interface: biotic-abiotic interactions between substrates and a model epithelium.” 2015. Doctoral Dissertation, University of North Carolina – Greensboro. Accessed September 15, 2019. http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=18887.

MLA Handbook (7^th Edition):

Covell, Alan D. “At the interface: biotic-abiotic interactions between substrates and a model epithelium.” 2015. Web. 15 Sep 2019.

Vancouver:

Covell AD. At the interface: biotic-abiotic interactions between substrates and a model epithelium. [Internet] [Doctoral dissertation]. University of North Carolina – Greensboro; 2015. [cited 2019 Sep 15]. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=18887.

Council of Science Editors:

Covell AD. At the interface: biotic-abiotic interactions between substrates and a model epithelium. [Doctoral Dissertation]. University of North Carolina – Greensboro; 2015. Available from: http://libres.uncg.edu/ir/listing.aspx?styp=ti&id=18887

University of New Mexico

10. Unione, Amelia H.T. The role of Bcl-2 modifying factor (Bmf) in airway epithelial cell death.

Degree: Biomedical Sciences Graduate Program, 2010, University of New Mexico

URL: https://digitalrepository.unm.edu/biom_etds/22

► One of the components that obstruct the airway in asthma is the sudden and increased secretion of mucus from metaplastic mucous cells in small airways.… (more)

▼ One of the components that obstruct the airway in asthma is the sudden and increased secretion of mucus from metaplastic mucous cells in small airways. Because previous studies have shown that the resolution of mucous cell metaplasia (MCM) during prolonged exposure of mice to allergen is mediated by IFN gamma and the Bcl-2 family of proteins, we investigated the regulation and the role of a pro-apoptotic BH3 domain-only protein, Bmf, in airway epithelial cells (AECs) treated with IFN gamma. We hypothesize that Bmf is crucial for IFN gamma-induced cell death. Our findings show that IFN gamma suppressed Bmf expression in a p53-dependent manner. IFN gamma treatment caused nuclear accumulation, increased association of p53 with HDAC1, the reduction of acetylated p53, and the interaction of p53 with the Bmf promoter. This reduction was primarily of the higher molecular weight Bmf that was found to increase cell colony formation in vitro. Bmf was important for the resolution of MCM during prolonged exposure to allergen because the mucous cell numbers did not decline in bmf-/- mice compared to wild-type controls during prolonged exposure to allergen. In addition, bmf-/- mouse airway epithelial cells (MAECs) were resistant to IFN gamma-induced cell death. Previous studies in cancer cell lines have shown that Bmf mediates cell death in response to histone deacetylase inhibitors (HDACis). We found that HDACis increased expression of Bmf in AECs through the displacement of HDAC1 and the acetylation of histones 3 and 4 associated with the Bmf promoter. Bmf-deficient AECs were resistant to HDACi-induced cell death, while expressing Bmf in the bmf-/- MAECs restored this cell death process demonstrating that Bmf is a critical mediator of this cell death process. In conclusion, these findings show that Bmf mediates IFN gamma- and HDACi-induced cell death in AECs and implies that HDACis may be useful for treatment of cancers and for reducing AEC hyperplasia and MCM, thereby reducing mucous hypersecretions and airway obstruction in chronic diseases. Advisors/Committee Members: Tesfaigzi, Yohannes, Hudson, Laurie, Belinsky, Steve, Hathaway, Helen, Wilson, Bridget.

Subjects/Keywords: airway epithelial cells; Bmf

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APA (6^th Edition):

Unione, A. H. T. (2010). The role of Bcl-2 modifying factor (Bmf) in airway epithelial cell death. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/22

Chicago Manual of Style (16^th Edition):

Unione, Amelia H T. “The role of Bcl-2 modifying factor (Bmf) in airway epithelial cell death.” 2010. Doctoral Dissertation, University of New Mexico. Accessed September 15, 2019. https://digitalrepository.unm.edu/biom_etds/22.

MLA Handbook (7^th Edition):

Unione, Amelia H T. “The role of Bcl-2 modifying factor (Bmf) in airway epithelial cell death.” 2010. Web. 15 Sep 2019.

Vancouver:

Unione AHT. The role of Bcl-2 modifying factor (Bmf) in airway epithelial cell death. [Internet] [Doctoral dissertation]. University of New Mexico; 2010. [cited 2019 Sep 15]. Available from: https://digitalrepository.unm.edu/biom_etds/22.

Council of Science Editors:

Unione AHT. The role of Bcl-2 modifying factor (Bmf) in airway epithelial cell death. [Doctoral Dissertation]. University of New Mexico; 2010. Available from: https://digitalrepository.unm.edu/biom_etds/22

University of Manitoba

11. Kroeker, Andrea. A proteomic approach to discovering novel anti-influenza mechanisms in primary human airway epithelial cells.

Degree: Physiology and Pathophysiology, 2012, University of Manitoba

URL: http://hdl.handle.net/1993/30400

► The influenza virus has a large impact on global health; however, it is difficult to formulate vaccines and influenza therapies that are effective against influenza.… (more)

Subjects/Keywords: influenza; proteomics; airway epithelial cells

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APA (6^th Edition):

Kroeker, A. (2012). A proteomic approach to discovering novel anti-influenza mechanisms in primary human airway epithelial cells. (Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/30400

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kroeker, Andrea. “A proteomic approach to discovering novel anti-influenza mechanisms in primary human airway epithelial cells.” 2012. Thesis, University of Manitoba. Accessed September 15, 2019. http://hdl.handle.net/1993/30400.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kroeker, Andrea. “A proteomic approach to discovering novel anti-influenza mechanisms in primary human airway epithelial cells.” 2012. Web. 15 Sep 2019.

Vancouver:

Kroeker A. A proteomic approach to discovering novel anti-influenza mechanisms in primary human airway epithelial cells. [Internet] [Thesis]. University of Manitoba; 2012. [cited 2019 Sep 15]. Available from: http://hdl.handle.net/1993/30400.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kroeker A. A proteomic approach to discovering novel anti-influenza mechanisms in primary human airway epithelial cells. [Thesis]. University of Manitoba; 2012. Available from: http://hdl.handle.net/1993/30400

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Waterloo

12. Li, Ziqing. Effects of Temperature on the Proliferation of Human and Fish Lens Epithelial Cells.

Degree: 2019, University of Waterloo

URL: http://hdl.handle.net/10012/14997

► Crystallins are proteins that confer refractive properties to the crystalline lens. All vertebrate lenses contain α- and β-crystallins, and often a third major crystallin. Crystallins… (more)

Subjects/Keywords: lens epithelial cells; crystallin; temperature

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APA (6^th Edition):

Li, Z. (2019). Effects of Temperature on the Proliferation of Human and Fish Lens Epithelial Cells. (Thesis). University of Waterloo. Retrieved from http://hdl.handle.net/10012/14997

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Li, Ziqing. “Effects of Temperature on the Proliferation of Human and Fish Lens Epithelial Cells.” 2019. Thesis, University of Waterloo. Accessed September 15, 2019. http://hdl.handle.net/10012/14997.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Li, Ziqing. “Effects of Temperature on the Proliferation of Human and Fish Lens Epithelial Cells.” 2019. Web. 15 Sep 2019.

Vancouver:

Li Z. Effects of Temperature on the Proliferation of Human and Fish Lens Epithelial Cells. [Internet] [Thesis]. University of Waterloo; 2019. [cited 2019 Sep 15]. Available from: http://hdl.handle.net/10012/14997.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Li Z. Effects of Temperature on the Proliferation of Human and Fish Lens Epithelial Cells. [Thesis]. University of Waterloo; 2019. Available from: http://hdl.handle.net/10012/14997

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Aberdeen

13. Sagga, Nada A. Dynamics of limbal and conjunctival stem cell activity during ocular surface maintenance.

Degree: PhD, 2017, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=235418 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.731630

► Corneal degenerative diseases and opacity are leading causes of corneal impairment and blindness worldwide. Like many epithelial tissues, the constant renewal of transparent corneal epithelial… (more)

▼ Corneal degenerative diseases and opacity are leading causes of corneal impairment and blindness worldwide. Like many epithelial tissues, the constant renewal of transparent corneal epithelial cells is essential for a lifelong healthy cornea and optimal vision. The limbus (the boundary between the cornea and the conjunctiva) is believed to be the site that harbours adult stem cells responsible for corneal maintenance and repair after injury, referred to as limbal epithelial stem cells (LESCs). In the basal limbal epithelium, an active LESC subset divides to yield progenitor cells that migrate centripetally into the corneal epithelium for cell renewal. This asymmetric division however, is assumed to be regulated by a balance between cell renewal and loss of cells from the corneal surface. The search for specific LESC molecular markers has been difficult and to date there are few if any candidate markers that unambiguously identify LESCs but not their immediate progeny. Consequently, LESC clonality, activity and proliferative dynamics have remained poorly understood. In addition, the nature of the regulatory molecular pathways involved during LESC activity is still an open key question. In this research project, we identified stem cells on the ocular surface of the eye, assayed their activity and demonstrated quantitively for the first time how the cornea responds to damage. The retention of DNA labelling reagents in control and wounded corneas was combined with clonal analyses of cell division and migration using mice mosaic for reporter LacZ expression. Corneal transplant in LacZ reporter transgenic mice showed migration of LacZ-positive cells into the donor corneal button, with long-term disruption of patterns of migration. Corneal epithelial scrape wounds at the periphery also showed long– term disruption. Label retention suggested a small but statistically significant proliferation response of LESCs to injury, but this was attenuated or absent in aging mice and Pax6 mutants. The Hippo signalling pathway has been shown to have promising results in regulating stem cell activity and proliferation in many organs, however, its effect on LESC proliferation is unknown. Here, we investigated the regulatory role of the Hippo−YAP signalling pathway during cell proliferation, and determined whether the label retention assay in a uniform population of dividing cells is a real indicator of slow-cycling cells in vivo. Cell-cycling kinetics, Abstract v proliferation rate, and label retention were determined in a spontaneous human corneal epithelial (HCE-S) cell line, using double-labelling IdU and EdU thymidine analogues. During homeostasis, HCE-S cells underwent approximately one cell cycle per day, however, cells in which YAP-dependent signalling was activated by 17-Allylamino-17-demethoxygeldanamycin (17-AAG), an inhibitor of heat shock protein 90 (Hsp90), showed slower proliferation rate and longer cell-cycle time. In vitro label-retention assay in confluent cultures estimated number of ~3-4 cell cycles needed to dilute out…

Subjects/Keywords: 610; Cornea; Epithelial cells; Stem cells

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APA (6^th Edition):

Sagga, N. A. (2017). Dynamics of limbal and conjunctival stem cell activity during ocular surface maintenance. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=235418 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.731630

Chicago Manual of Style (16^th Edition):

Sagga, Nada A. “Dynamics of limbal and conjunctival stem cell activity during ocular surface maintenance.” 2017. Doctoral Dissertation, University of Aberdeen. Accessed September 15, 2019. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=235418 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.731630.

MLA Handbook (7^th Edition):

Sagga, Nada A. “Dynamics of limbal and conjunctival stem cell activity during ocular surface maintenance.” 2017. Web. 15 Sep 2019.

Vancouver:

Sagga NA. Dynamics of limbal and conjunctival stem cell activity during ocular surface maintenance. [Internet] [Doctoral dissertation]. University of Aberdeen; 2017. [cited 2019 Sep 15]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=235418 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.731630.

Council of Science Editors:

Sagga NA. Dynamics of limbal and conjunctival stem cell activity during ocular surface maintenance. [Doctoral Dissertation]. University of Aberdeen; 2017. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=235418 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.731630

Georgia Tech

14. Enemchukwu, Nduka Obichukwu. Bioartificial matrices to modulate epithelial morphogenesis.

Degree: PhD, Mechanical Engineering, 2013, Georgia Tech

URL: http://hdl.handle.net/1853/52938

► Acute injury of major epithelial organ systems (kidney, liver, lung, etc.) is collectively a principal cause of death worldwide. Regenerative medicine promises to meet these… (more)

▼ Acute injury of major epithelial organ systems (kidney, liver, lung, etc.) is collectively a principal cause of death worldwide. Regenerative medicine promises to meet these human health challenges by harnessing intrinsic cellular processes to repair or replace damaged tissues. Epithelial morphogenesis is a hard-wired, multicellular differentiation program that dynamically integrates microenvironmental cues to coordinate cell fate processes including adhesion, migration, proliferation, and polarization. Thus, epithelial morphogenesis is an instructive mode of tissue assembly, maintenance, and repair. Three-dimensional epithelial cell cultures in natural basement membrane (BM) extracts produce hollow, spherical cyst structures and have indicated that the BM provides the critical cell adhesion ligands to facilitate cell survival, stimulate proliferation, and promote polarization and lumen formation. However, the utility of natural BMs for detailed studies is generally limited by lot-to-lot variations, uncontrolled cell adhesive interactions, or growth factor contamination. The goal of this thesis was to engineer bioartificial extracellular matrices (ECM) that would support and modulate epithelial cyst morphogenesis. We have engineered hydrogels, based on a multi-arm maleimide-terminated poly (ethylene glycol) (PEG-4MAL), that present cell adhesive molecules and enzymatic degradation substrates and promote polarized epithelial cyst differentiation in vitro. To investigate the influence of matrix physical and biochemical signals on cyst morphogenesis, we independently varied the polymer weight percentage (wt%), the density of a cell adhesion ligand (RGD), and crosslink degradation rates of the hydrogels. Then, we evaluated functional outcomes including Madin-Darby canine kidney (MDCK II) epithelial cell survival, proliferation, cyst polarization, and lumen formation. We found that cell proliferation, but not cell survival, was sensitive to the polymer wt%, which is related to elastic modulus and crosslink density. This result defined a working range of PEG-4MAL concentration (3.5% - 4.5%) that promotes robust proliferation. Analysis of mature cysts indicated that 4.0% and 4.5% gels produced cysts resembling those typically grown in type I collagen gels while 3.5% gels produced cysts with higher incidence of inverted polarity and multiple lumens. Perturbation of matrix degradability using a slow-degrading crosslink peptide or matrix metalloproteinase inhibitors showed that the rate of matrix degradation exerts major influence on cyst growth in PEG-4MAL gels. We employed 4.0% PEG-4MAL hydrogels with RGD ligand density ranging over 0 – 2000 uM to discover that (1) lumen formation was eliminated in the absence of RGD, (2) extent of lumen formation increased with increasing RGD concentration, and (3) cyst polarity was inverted below a threshold of integrin binding to RGD. Together, these results show that the biochemical and physical properties of the matrix, particularly integrin binding and matrix degradability,… Advisors/Committee Members: García, Andrés (advisor), Nusrat, Asma (committee member), Barker, Thomas H. (committee member), Collard, David M. (committee member), Dixon, J. Brandon (committee member).

Subjects/Keywords: Biomaterials; Polyethylene glycol; Epithelial morphogenesis; Cyst; Extracellular matrix; Epithelial cells

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APA (6^th Edition):

Enemchukwu, N. O. (2013). Bioartificial matrices to modulate epithelial morphogenesis. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/52938

Chicago Manual of Style (16^th Edition):

Enemchukwu, Nduka Obichukwu. “Bioartificial matrices to modulate epithelial morphogenesis.” 2013. Doctoral Dissertation, Georgia Tech. Accessed September 15, 2019. http://hdl.handle.net/1853/52938.

MLA Handbook (7^th Edition):

Enemchukwu, Nduka Obichukwu. “Bioartificial matrices to modulate epithelial morphogenesis.” 2013. Web. 15 Sep 2019.

Vancouver:

Enemchukwu NO. Bioartificial matrices to modulate epithelial morphogenesis. [Internet] [Doctoral dissertation]. Georgia Tech; 2013. [cited 2019 Sep 15]. Available from: http://hdl.handle.net/1853/52938.

Council of Science Editors:

Enemchukwu NO. Bioartificial matrices to modulate epithelial morphogenesis. [Doctoral Dissertation]. Georgia Tech; 2013. Available from: http://hdl.handle.net/1853/52938

University of Bath

15. Doughton, Gail Louise. Cell fate specification and polarisation in mouse preimplantation epithelia.

Degree: PhD, 2014, University of Bath

URL: https://researchportal.bath.ac.uk/en/studentthesis/cell-fate-specification-and-polarisation-in-mouse-preimplantation-epithelia(d8fbae5b-285b-4413-b370-3aa32ad4d607).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619153

► Understanding the establishment of polarity and the cell fate specification of epithelial cells is important for developmental biology, regenerative medicine and the study of cancer.… (more)

▼ Understanding the establishment of polarity and the cell fate specification of epithelial cells is important for developmental biology, regenerative medicine and the study of cancer. In this thesis, models of pre-implantation epithelial development are used to investigate the relationship between these two processes. The trophoblast is an extraembryonic epithelial tissue which contributes to the placenta. Addition of BMP4 to mouse and human embryonic stem (mES) cells grown in culture has been suggested to induce differentiation of cells to the trophoblast lineage. The use of this differentiation method was investigated as a possible model of trophoblast polarisation and cell fate specification. Unfortunately, with the protocol and reagents available this model did not appear to physiologically recapitulate trophoblast development and was not reliable. The primitive endoderm is an epithelium which arises from the inner cell mass during mammalian pre-implantation development. It faces the blastocoel cavity and later gives rise to the extraembryonic parietal and visceral endoderm. When mES cells are grown in suspension they form aggregates of differentiating cells known as embryoid bodies. The outermost cell layer of an embryoid body is an epithelial cell type comparable to the primitive endoderm. Embryoid bodies were used here to study the polarisation and cell fate specification of the primitive endoderm. The outer cells of these embryoid bodies were found to gradually acquire the hallmarks of polarised epithelial cells and express markers of primitive endoderm cell fate. The acquisition of epithelial polarity occurred prior to the maximal expression of cell fate markers. Fgfr/Erk signalling is known to be required for specification of the primitive endoderm, but its role in polarisation of this tissue is less well understood. To investigate the function of this pathway in the primitive endoderm, embryoid bodies were cultured in the presence of a small molecule inhibitor of Mek. This inhibitor caused a loss of expression of markers of primitive endoderm cell fate and maintenance of the pluripotency marker Nanog. In addition, a mislocalisation of apico-basolateral markers and disruption of the epithelial barrier which normally blocks free diffusion across the epithelial cell layer occurred. Two inhibitors of the Fgf receptor elicited similar phenotypes, suggesting that Fgf receptor signalling promotes Erkmediated polarisation. This data shows that the formation of a polarised primitive endoderm layer in embryoid bodies requires the Fgfr/Erk signalling pathway.

Subjects/Keywords: 611.0187; stem cells; Development; preimplantation embryo; epithelial polarity; epithelial

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Doughton, G. L. (2014). Cell fate specification and polarisation in mouse preimplantation epithelia. (Doctoral Dissertation). University of Bath. Retrieved from https://researchportal.bath.ac.uk/en/studentthesis/cell-fate-specification-and-polarisation-in-mouse-preimplantation-epithelia(d8fbae5b-285b-4413-b370-3aa32ad4d607).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619153

Chicago Manual of Style (16^th Edition):

Doughton, Gail Louise. “Cell fate specification and polarisation in mouse preimplantation epithelia.” 2014. Doctoral Dissertation, University of Bath. Accessed September 15, 2019. https://researchportal.bath.ac.uk/en/studentthesis/cell-fate-specification-and-polarisation-in-mouse-preimplantation-epithelia(d8fbae5b-285b-4413-b370-3aa32ad4d607).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619153.

MLA Handbook (7^th Edition):

Doughton, Gail Louise. “Cell fate specification and polarisation in mouse preimplantation epithelia.” 2014. Web. 15 Sep 2019.

Vancouver:

Doughton GL. Cell fate specification and polarisation in mouse preimplantation epithelia. [Internet] [Doctoral dissertation]. University of Bath; 2014. [cited 2019 Sep 15]. Available from: https://researchportal.bath.ac.uk/en/studentthesis/cell-fate-specification-and-polarisation-in-mouse-preimplantation-epithelia(d8fbae5b-285b-4413-b370-3aa32ad4d607).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619153.

Council of Science Editors:

Doughton GL. Cell fate specification and polarisation in mouse preimplantation epithelia. [Doctoral Dissertation]. University of Bath; 2014. Available from: https://researchportal.bath.ac.uk/en/studentthesis/cell-fate-specification-and-polarisation-in-mouse-preimplantation-epithelia(d8fbae5b-285b-4413-b370-3aa32ad4d607).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619153

The Ohio State University

16. Lehman, Teresa Ann. Studies in human skin epithelial cell carcinogenesis .

Degree: PhD, Graduate School, 1987, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1487332636474889

Subjects/Keywords: Chemistry; Epithelial cells

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APA (6^th Edition):

Lehman, T. A. (1987). Studies in human skin epithelial cell carcinogenesis . (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1487332636474889

Chicago Manual of Style (16^th Edition):

Lehman, Teresa Ann. “Studies in human skin epithelial cell carcinogenesis .” 1987. Doctoral Dissertation, The Ohio State University. Accessed September 15, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487332636474889.

MLA Handbook (7^th Edition):

Lehman, Teresa Ann. “Studies in human skin epithelial cell carcinogenesis .” 1987. Web. 15 Sep 2019.

Vancouver:

Lehman TA. Studies in human skin epithelial cell carcinogenesis . [Internet] [Doctoral dissertation]. The Ohio State University; 1987. [cited 2019 Sep 15]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1487332636474889.

Council of Science Editors:

Lehman TA. Studies in human skin epithelial cell carcinogenesis . [Doctoral Dissertation]. The Ohio State University; 1987. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1487332636474889

Texas A&M University

17. Pedrigi, Ryan M. Biomechanics of the Lens Capsule from Native to After Cataract Surgery.

Degree: 2010, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-2008-08-40

► The primary function of the lens capsule of the eye unfolds during the process of accommodation; wherein, tension imposed onto its equator is released, allowing… (more)

Subjects/Keywords: Capsulorhexis; Lens Epithelial Cells; Mechanical Properties

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APA (6^th Edition):

Pedrigi, R. M. (2010). Biomechanics of the Lens Capsule from Native to After Cataract Surgery. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2008-08-40

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Pedrigi, Ryan M. “Biomechanics of the Lens Capsule from Native to After Cataract Surgery.” 2010. Thesis, Texas A&M University. Accessed September 15, 2019. http://hdl.handle.net/1969.1/ETD-TAMU-2008-08-40.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Pedrigi, Ryan M. “Biomechanics of the Lens Capsule from Native to After Cataract Surgery.” 2010. Web. 15 Sep 2019.

Vancouver:

Pedrigi RM. Biomechanics of the Lens Capsule from Native to After Cataract Surgery. [Internet] [Thesis]. Texas A&M University; 2010. [cited 2019 Sep 15]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2008-08-40.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Pedrigi RM. Biomechanics of the Lens Capsule from Native to After Cataract Surgery. [Thesis]. Texas A&M University; 2010. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2008-08-40

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

The Ohio State University

18. Zikri, Nancy N. A study of the chemopreventive effects of black raspberry components in rat esophageal epithelial cells.

Degree: PhD, Public Health, 2008, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1198691632

► Our laboratory has demonstrated the preventive effects of freeze-dried black raspberries 0028BRB0029 on tumor development in the rat esophagus and colon in vivo. In attempts… (more)

▼ Our laboratory has demonstrated the preventive effects of freeze-dried black raspberries 0028BRB0029 on tumor development in the rat esophagus and colon in vivo. In attempts to explain these inhibitory effects, we tested two BRB extracts and two component anthocyanins 0028cyanidin-3-O-glucoside and cyanidin-3-O-rutinoside0029 in BRB for their effects on growth, apoptosis and gene expression in weakly tumorigenic 0028RE-1490029 and highly tumorigenic 0028RE-149 DHD0029 rat esophageal cell lines. The ethanol 0028EtOH0029 extract 0028100 00B5g/ml0029 and both anthocyanins 002850 00B5g/ml0029 had a selective growth-inhibitory pattern similar to that of both extracts. The EtOH extract and cyanidin-3-O-rutinoside induced capsases 3 and 7 activities significantly in RE-149 DHD cells. The growth inhibitory and the pro-apoptotic effects were enhanced by the daily addition of the EtOH extract and the anthocyanins to the medium. Maximal uptake of the anthocyanins in the EtOH extract by RE-149 DHD cells occurred after 1 hour of extract treatment followed by a rapid loss of anthocyanins from the cells. The uptake of anthocyanins by RE-149 cells had the same pattern as RE-149 DHD cells, but the amount of anthocyanins taken up was 100 times lower. This finding might explain the difference in the inhibitory effect of EtOH extract in both cell lines. Using DNA microarray technique, the EtOH extract was found to down-regulate multiple genes associated with esophageal tumors. The calcium signaling pathway was a major pathway modulated by the extract since several genes were down-regulated and all of them are linked to calcium, and all are involved in tumor development and progression in several organ sites.These genes include: calmodulin kinase II 0028CaMKII0029, protein kinase C iota 0028PKC03B90029, MAPK 9, and Cdc 25 a and b. The EtOH extract was found to down-regulate 16 genes consistently including: SERCA2a which functions as a calcium pump, fibroblast growth factor receptor 2, insulin-like growth factor binding protein 5, secreted protein acidic and rich in cysteine 0028SPARC0029, and galanin, all of which were demonstrated to play crucial roles in tumor development in multiple organs including the esophagus. Advisors/Committee Members: Stoner, Gary (Advisor).

Subjects/Keywords: Black raspberry; rat esophageal epithelial cells; anthocyanins

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APA (6^th Edition):

Zikri, N. N. (2008). A study of the chemopreventive effects of black raspberry components in rat esophageal epithelial cells. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1198691632

Chicago Manual of Style (16^th Edition):

Zikri, Nancy N. “A study of the chemopreventive effects of black raspberry components in rat esophageal epithelial cells.” 2008. Doctoral Dissertation, The Ohio State University. Accessed September 15, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1198691632.

MLA Handbook (7^th Edition):

Zikri, Nancy N. “A study of the chemopreventive effects of black raspberry components in rat esophageal epithelial cells.” 2008. Web. 15 Sep 2019.

Vancouver:

Zikri NN. A study of the chemopreventive effects of black raspberry components in rat esophageal epithelial cells. [Internet] [Doctoral dissertation]. The Ohio State University; 2008. [cited 2019 Sep 15]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1198691632.

Council of Science Editors:

Zikri NN. A study of the chemopreventive effects of black raspberry components in rat esophageal epithelial cells. [Doctoral Dissertation]. The Ohio State University; 2008. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1198691632

Universiteit Utrecht

19. Cook, E.C.L. The Expression of RALDH Enzymes by Small Intestinal Epithelial Cells.

Degree: 2012, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/233670

► Retinal dehydrogenase (RALDH) is the key enzyme that regulates the production of retinoic acid (RA), an important mediator of immune responses in the gut. RA… (more)

Subjects/Keywords: RALDH; intestinal epithelial cells; vitamin A; retinol

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APA (6^th Edition):

Cook, E. C. L. (2012). The Expression of RALDH Enzymes by Small Intestinal Epithelial Cells. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/233670

Chicago Manual of Style (16^th Edition):

Cook, E C L. “The Expression of RALDH Enzymes by Small Intestinal Epithelial Cells.” 2012. Masters Thesis, Universiteit Utrecht. Accessed September 15, 2019. http://dspace.library.uu.nl:8080/handle/1874/233670.

MLA Handbook (7^th Edition):

Cook, E C L. “The Expression of RALDH Enzymes by Small Intestinal Epithelial Cells.” 2012. Web. 15 Sep 2019.

Vancouver:

Cook ECL. The Expression of RALDH Enzymes by Small Intestinal Epithelial Cells. [Internet] [Masters thesis]. Universiteit Utrecht; 2012. [cited 2019 Sep 15]. Available from: http://dspace.library.uu.nl:8080/handle/1874/233670.

Council of Science Editors:

Cook ECL. The Expression of RALDH Enzymes by Small Intestinal Epithelial Cells. [Masters Thesis]. Universiteit Utrecht; 2012. Available from: http://dspace.library.uu.nl:8080/handle/1874/233670

University of Western Australia

20. Stevens, Paul. Intrinsic differences of the airway epithelium in childhood allergic asthma.

Degree: PhD, 2009, University of Western Australia

URL: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=12702&local_base=GEN01-INS01

► [Truncated abstract] Asthma affects millions of people worldwide and places a substantial burden on the healthcare system. Despite advances in our understanding of disease mechanisms… (more)

▼ [Truncated abstract] Asthma affects millions of people worldwide and places a substantial burden on the healthcare system. Despite advances in our understanding of disease mechanisms and the role of respiratory viruses in asthma exacerbations, there is little known regarding the role of the epithelium in commonly observed structural changes in the airway wall. The epithelium of the airways provides an essential protective barrier between the environment and underlying structures and is responsible for the secretion of diverse compounds. Since it is likely that dysregulated epithelial characteristics and function in childhood asthma are critical determinants of disease progression in adults, it is pertinent to investigate the cellular mechanisms involved in paediatric asthma. However, full comprehension of paediatric respiratory diseases and the childhood antecedents of adult respiratory disease are currently hampered by the difficulty in obtaining relevant target organ tissue and most of the data to date have been generated from studies involving adults or commercially derived cell lines. This laboratory has successfully developed methodologies of obtaining and studying samples of paediatric primary airway epithelial cells (pAECs) and has identified significant biochemical and functional differences between healthy non-atopic (pAECHNA) and atopic asthmatic (pAECAA) airway cells, which have assisted in the identification of potential mechanisms responsible for abnormal epithelial function. Stevens 2009 ... Exposure of pAECs with RV resulted in elevated PAI-1 mRNA expression and reduced MMP-9 release in both pAECAA and pAECHNA samples. Collectively, the data presented indicate that RV exposure induces a pronounced antiproliferative and retardative repair effect in pAECAA and that the presence of virus may have a role in the PAI-1 and MMP expression witnessed in these cells. In conclusion, this investigation has further characterised the essential role the airway epithelium plays in childhood asthma by demonstrating for the first time that pAECs from asthmatic children lack the ability to successfully repair mechanically induced wounds. This investigation also showed that PAI-1 is elevated in pAECAA and has a functional role in the pAEC proliferative and regenerative processes. It was demonstrated that MMP-2 and MMP-9 activities and the MMP-9/TIMP-1 as well as MMP2/TIMP2 ratios were significantly reduced in pAECAA thereby providing additional evidence that there is a dysregulation in the mechanisms that monitor the turnover of the ECM in childhood asthma. Furthermore, this study has shown for the first time that pAECs from untreated mild atopic-asthmatic children are more sensitive to the pathogenic effects of RV than healthy control cells and that RV exposure delays cellular proliferation and repair. Ultimately, these findings support the hypothesis postulated and provide evidence that indeed the dysregulated epithelial functional characteristics seen in childhood mild asthma may be a critical determinant of disease…

Subjects/Keywords: Asthma in children; Epithelial cells; Asthma; Epithelium

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APA (6^th Edition):

Stevens, P. (2009). Intrinsic differences of the airway epithelium in childhood allergic asthma. (Doctoral Dissertation). University of Western Australia. Retrieved from http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=12702&local_base=GEN01-INS01

Chicago Manual of Style (16^th Edition):

Stevens, Paul. “Intrinsic differences of the airway epithelium in childhood allergic asthma.” 2009. Doctoral Dissertation, University of Western Australia. Accessed September 15, 2019. http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=12702&local_base=GEN01-INS01.

MLA Handbook (7^th Edition):

Stevens, Paul. “Intrinsic differences of the airway epithelium in childhood allergic asthma.” 2009. Web. 15 Sep 2019.

Vancouver:

Stevens P. Intrinsic differences of the airway epithelium in childhood allergic asthma. [Internet] [Doctoral dissertation]. University of Western Australia; 2009. [cited 2019 Sep 15]. Available from: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=12702&local_base=GEN01-INS01.

Council of Science Editors:

Stevens P. Intrinsic differences of the airway epithelium in childhood allergic asthma. [Doctoral Dissertation]. University of Western Australia; 2009. Available from: http://repository.uwa.edu.au:80/R/?func=dbin-jump-full&object_id=12702&local_base=GEN01-INS01

University of Aberdeen

21. Findlay, Amy Siobhan. The molecular basis of epthelial cell migration : maintenance and repair of the ocular surface.

Degree: PhD, 2015, University of Aberdeen

URL: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=228963 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.680985

► In vertebrates the cornea must maintain its transparency throughout adult life to ensure sight, and understanding the mechanisms underpinning corneal homeostasis are fundamental to developing… (more)

Subjects/Keywords: 610; Cornea; Epithelial cells; Cell migration; Homeostasis

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APA (6^th Edition):

Findlay, A. S. (2015). The molecular basis of epthelial cell migration : maintenance and repair of the ocular surface. (Doctoral Dissertation). University of Aberdeen. Retrieved from http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=228963 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.680985

Chicago Manual of Style (16^th Edition):

Findlay, Amy Siobhan. “The molecular basis of epthelial cell migration : maintenance and repair of the ocular surface.” 2015. Doctoral Dissertation, University of Aberdeen. Accessed September 15, 2019. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=228963 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.680985.

MLA Handbook (7^th Edition):

Findlay, Amy Siobhan. “The molecular basis of epthelial cell migration : maintenance and repair of the ocular surface.” 2015. Web. 15 Sep 2019.

Vancouver:

Findlay AS. The molecular basis of epthelial cell migration : maintenance and repair of the ocular surface. [Internet] [Doctoral dissertation]. University of Aberdeen; 2015. [cited 2019 Sep 15]. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=228963 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.680985.

Council of Science Editors:

Findlay AS. The molecular basis of epthelial cell migration : maintenance and repair of the ocular surface. [Doctoral Dissertation]. University of Aberdeen; 2015. Available from: http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=228963 ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.680985

University of Hong Kong

22. So, Kam-hei. Role of human chorionic gonadotropin (HCG) on embryo attachment onto oviductal epithelial cells through downregulation of olfactomedin-1 (OLFM1).

Degree: PhD, 2015, University of Hong Kong

URL: So, K. [蘇錦熙]. (2015). Role of human chorionic gonadotropin (HCG) on embryo attachment onto oviductal epithelial cells through downregulation of olfactomedin-1 (OLFM1). (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5719484 ; http://hdl.handle.net/10722/223578

► Tubal ectopic pregnancy (TEP) occurs in 2% of pregnancy and is potentially fatal to pregnant women because of the risk of Fallopian tube/oviduct rupture. The… (more)

▼ Tubal ectopic pregnancy (TEP) occurs in 2% of pregnancy and is potentially fatal to pregnant women because of the risk of Fallopian tube/oviduct rupture. The causes of ectopic pregnancy are associated with pelvic infection, tobacco smoking and the use of assisted reproductive technology. However, the underlying mechanism leading to TEP remains largely unknown. Results from recent studies suggested that human chorionic gonadotrophin (hCG) stimulates miRNA expression in female reproductive tract and miRNAs play important roles on various biological processes. In silico analysis identified miRNA-212 may regulate Olfactomedin-1 (Olfm1) expression which was found to be down-regulated in endometrial epithelium during embryo implantation. Therefore, we hypothesized that embryo-derived hCG stimulates miRNA-212 expression, down-regulated Olfm1 expression in the Fallopian epithelium and favor embryo attachment leading to ectopic pregnancy. Furthermore, the effect of hCG binding onto LH/CG receptor (LH/CGR) and the downstream protein kinase and Wnt signaling pathways was investigated. It was found that Olfm1 was down-regulated and LH/CGR was up-regulated at the luteal phase of the menstrual cycle in the human Fallopian tube. hCG (25IU/ml) down-regulated Olfm1 in human oviductal epithelial cells (OE-E6/E7). Both hCG (25IU/ml) and hCG beta subunit increased JAR spheroids (blastocyst surrogate) attachment rate onto OE-E6/E7 cells. Knockdown of LH/CGR siRNA reduces, while knockdown of Olfm1 siRNA increases spheroids attachment, respectively. Progesterone (60nM) increased attachment rate and up-regulated the expression of LH/CGR. LH/CGR could activate its downstream signaling pathways through either protein kinase A or protein kinase C. PKA activator (Forskolin) has no effect on spheroid attachment; while PKC activator (PMA) increased attachment rate, suggesting hCG promotes spheroids attachment through PKC signaling pathway. Furthermore, hCG activates Erk and Wnt signaling pathways; while knockdown of LH/CGR abolished the effect of hCG on Erk activation in OE-E6/E7 cells. Similarly, Erk or Wnt activator down-regulated Olfm1, while Erk or Wnt inhibitor up-regulated Olfm1 expression and stimulates spheroid attachment in OE-E6/E7 cells. In line with this, immunohistochemistry of human Fallopian tubes obtained from ectopic pregnancy and normal non-pregnant women showed activation of Erk signaling pathway in the epithelium of TEP samples. In silico analysis of the promoter region of hsa-miR212 revealed binding site of LEF-1, a Wnt signaling transcriptional factor. Chromatin immunoprecipitaiton showed binding of LEF-1 to the promoter region of hsa-miR212. Hsa-miR212 mimic down-regulated Olfm1 and promoted spheroids attachment; while hsa-miR212 inhibitor up-regulated Olfm1 and suppressed spheroids attachment. To summarize, our results demonstrated that hCG (25IU/ml) act through LH/CGR, activates Erk and Wnt signaling pathways, induces miR-212 expression and down-regulates Olfm1, which favors embryo attached onto oviductal…

Subjects/Keywords: Oviduct; Embryology, Human; Chorionic gonadotropins; Epithelial cells

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APA (6^th Edition):

So, K. (2015). Role of human chorionic gonadotropin (HCG) on embryo attachment onto oviductal epithelial cells through downregulation of olfactomedin-1 (OLFM1). (Doctoral Dissertation). University of Hong Kong. Retrieved from So, K. [蘇錦熙]. (2015). Role of human chorionic gonadotropin (HCG) on embryo attachment onto oviductal epithelial cells through downregulation of olfactomedin-1 (OLFM1). (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5719484 ; http://hdl.handle.net/10722/223578

Chicago Manual of Style (16^th Edition):

So, Kam-hei. “Role of human chorionic gonadotropin (HCG) on embryo attachment onto oviductal epithelial cells through downregulation of olfactomedin-1 (OLFM1).” 2015. Doctoral Dissertation, University of Hong Kong. Accessed September 15, 2019. So, K. [蘇錦熙]. (2015). Role of human chorionic gonadotropin (HCG) on embryo attachment onto oviductal epithelial cells through downregulation of olfactomedin-1 (OLFM1). (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5719484 ; http://hdl.handle.net/10722/223578.

MLA Handbook (7^th Edition):

So, Kam-hei. “Role of human chorionic gonadotropin (HCG) on embryo attachment onto oviductal epithelial cells through downregulation of olfactomedin-1 (OLFM1).” 2015. Web. 15 Sep 2019.

Vancouver:

So K. Role of human chorionic gonadotropin (HCG) on embryo attachment onto oviductal epithelial cells through downregulation of olfactomedin-1 (OLFM1). [Internet] [Doctoral dissertation]. University of Hong Kong; 2015. [cited 2019 Sep 15]. Available from: So, K. [蘇錦熙]. (2015). Role of human chorionic gonadotropin (HCG) on embryo attachment onto oviductal epithelial cells through downregulation of olfactomedin-1 (OLFM1). (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5719484 ; http://hdl.handle.net/10722/223578.

Council of Science Editors:

So K. Role of human chorionic gonadotropin (HCG) on embryo attachment onto oviductal epithelial cells through downregulation of olfactomedin-1 (OLFM1). [Doctoral Dissertation]. University of Hong Kong; 2015. Available from: So, K. [蘇錦熙]. (2015). Role of human chorionic gonadotropin (HCG) on embryo attachment onto oviductal epithelial cells through downregulation of olfactomedin-1 (OLFM1). (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5719484 ; http://hdl.handle.net/10722/223578

University of Hong Kong

23. Wan, Shek-kong, Thomas. Establishment and characterization of human ovarian surface epithelialcells immortalized by human papilloma viral oncogenes.

Degree: PhD, 1997, University of Hong Kong

URL: Wan, S. T. [溫錫剛]. (1997). Establishment and characterization of human ovarian surface epithelial cells immortalized by human papilloma viral oncogenes. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b3123623 ; http://dx.doi.org/10.5353/th_b3123623 ; http://hdl.handle.net/10722/34849

published_or_final_version

Anatomy

Doctoral

Doctor of Philosophy

Subjects/Keywords: Oncogenes.; Epithelial cells.

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APA (6^th Edition):

Wan, Shek-kong, T. (1997). Establishment and characterization of human ovarian surface epithelialcells immortalized by human papilloma viral oncogenes. (Doctoral Dissertation). University of Hong Kong. Retrieved from Wan, S. T. [溫錫剛]. (1997). Establishment and characterization of human ovarian surface epithelial cells immortalized by human papilloma viral oncogenes. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b3123623 ; http://dx.doi.org/10.5353/th_b3123623 ; http://hdl.handle.net/10722/34849

Chicago Manual of Style (16^th Edition):

Wan, Shek-kong, Thomas. “Establishment and characterization of human ovarian surface epithelialcells immortalized by human papilloma viral oncogenes.” 1997. Doctoral Dissertation, University of Hong Kong. Accessed September 15, 2019. Wan, S. T. [溫錫剛]. (1997). Establishment and characterization of human ovarian surface epithelial cells immortalized by human papilloma viral oncogenes. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b3123623 ; http://dx.doi.org/10.5353/th_b3123623 ; http://hdl.handle.net/10722/34849.

MLA Handbook (7^th Edition):

Wan, Shek-kong, Thomas. “Establishment and characterization of human ovarian surface epithelialcells immortalized by human papilloma viral oncogenes.” 1997. Web. 15 Sep 2019.

Vancouver:

Wan, Shek-kong T. Establishment and characterization of human ovarian surface epithelialcells immortalized by human papilloma viral oncogenes. [Internet] [Doctoral dissertation]. University of Hong Kong; 1997. [cited 2019 Sep 15]. Available from: Wan, S. T. [溫錫剛]. (1997). Establishment and characterization of human ovarian surface epithelial cells immortalized by human papilloma viral oncogenes. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b3123623 ; http://dx.doi.org/10.5353/th_b3123623 ; http://hdl.handle.net/10722/34849.

Council of Science Editors:

Wan, Shek-kong T. Establishment and characterization of human ovarian surface epithelialcells immortalized by human papilloma viral oncogenes. [Doctoral Dissertation]. University of Hong Kong; 1997. Available from: Wan, S. T. [溫錫剛]. (1997). Establishment and characterization of human ovarian surface epithelial cells immortalized by human papilloma viral oncogenes. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b3123623 ; http://dx.doi.org/10.5353/th_b3123623 ; http://hdl.handle.net/10722/34849

Hong Kong University of Science and Technology

24. Li, Youjun. Epithelial cell growth and polarity establishment.

Degree: 2015, Hong Kong University of Science and Technology

URL: https://doi.org/10.14711/thesis-b1449009 ; http://repository.ust.hk/ir/bitstream/1783.1-87439/1/th_redirect.html

► The apical transmembrane protein Crumbs (Crb) is evolutionarily conserved in metazoan, and acts as a master cell polarity and growth regulator in polarized epithelia. Crb… (more)

▼ The apical transmembrane protein Crumbs (Crb) is evolutionarily conserved in metazoan, and acts as a master cell polarity and growth regulator in polarized epithelia. Crb intra-cellular functions are mediated by its highly conserved 37-residue cytoplasmic tail (Crb-CT). However, the mechanistic basis governing Crb's role in cell polarity and growth remains unclear. Here, I discover that the PDZ-SH3-GK tandem of PALS1 directly binds to Crb-CT with a dissociation constant of 70 nM, which is -100-fold stronger than the PALSI PDZ/Crb-CT interaction. The crystal structure of the PALS1 PDZ-SH3-GK/Crb-CT complex reveals that the PDZ-SH3-GK forms a structural supramodule with all three domains contributing to the tight binding to Crb. Mutations disrupting the tertiary interactions of the PDZ-SH3-GK supramodule weaken the PALSl/Crb interaction and compromise PALSI-mediated polarity establishment in MDCK cysts. These findings not only elucidate the molecular basis regard to Crb/PALSl complex in determining the apical-basal cell polarity, but also indicate a common PDZ-SH3-GK mode for other members of MAGUKs in specific target recognition. I also biochemically and structurally characterized the direct interaction between Crb-CT and Moesin FERM domain, which provides a direct linkage from the plasma membrane to the actin cytoskeleton. The 1.5 Å resolution crystal structure of the Moesin-FERM/Crb-CT complex reveals a typical FERM/FBM binding mode, in which the FBM of Crb-CT forms a short β-sheet and fits into the canonical F3-binding site. To our surprise, the PBM of Crb-CT also contributes to the binding to Moesin-FERM, by occupying the InsP₃ binding site at the Fl/F3 cleft, implying that Crb-CT may mimic the role of Ptdlns(4,5)P₂ in the activation of the ERM family proteins. Interestingly, phosphorylation of Crb-CT by aPKC disrupts the Crb/Moesin association, but has no impact on the Crb/PALSl interaction. The above findings suggest that establishment of cell polarity promotes aPKC-mediated Crb phosphorylation and subsequent Crb/Moesin complex dissociation. Thus, Crb becomes to be stably associated with tight junction-localized PALS1 in polarized epithelia. It is likely that aPKC-mediated phosphorylation of Crb functions to switch epithelial cells from proliferation to contact-mediated growth inhibition. Actin cytoskeleton is a major regulator of the Hippo signaling pathway, and angiomotin (AMOT) can relay the signals initiated by F-actin structural changes to control YAP activity. I show in the fourth part of this dissertation and by high resolution crystal structures that the Lats1/2 binding site on the Merlin FERM domain is physically blocked by Merlin's auto-inhibitory tail. AMOT binding releases the auto-inhibition and promotes Merlin's binding to Lats1/2. Phosphorylation of Ser518 outside the Merlin's auto-inhibitory tail prevents AMOT from binding, and thus inhibits Hippo kinase activation. These findings reveal that AMOT and Merlin interface the cortical actin filaments and the…

Subjects/Keywords: Epithelial cells; Growth; Cytoplasm; Membrane proteins; Structure

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Li, Y. (2015). Epithelial cell growth and polarity establishment. (Thesis). Hong Kong University of Science and Technology. Retrieved from https://doi.org/10.14711/thesis-b1449009 ; http://repository.ust.hk/ir/bitstream/1783.1-87439/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Li, Youjun. “Epithelial cell growth and polarity establishment.” 2015. Thesis, Hong Kong University of Science and Technology. Accessed September 15, 2019. https://doi.org/10.14711/thesis-b1449009 ; http://repository.ust.hk/ir/bitstream/1783.1-87439/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Li, Youjun. “Epithelial cell growth and polarity establishment.” 2015. Web. 15 Sep 2019.

Vancouver:

Li Y. Epithelial cell growth and polarity establishment. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2015. [cited 2019 Sep 15]. Available from: https://doi.org/10.14711/thesis-b1449009 ; http://repository.ust.hk/ir/bitstream/1783.1-87439/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Li Y. Epithelial cell growth and polarity establishment. [Thesis]. Hong Kong University of Science and Technology; 2015. Available from: https://doi.org/10.14711/thesis-b1449009 ; http://repository.ust.hk/ir/bitstream/1783.1-87439/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Hong Kong University of Science and Technology

25. Xie, Changyan LIFS. Mechanosensitive gating of CFTR in epithelial cell volume regulation.

Degree: 2014, Hong Kong University of Science and Technology

URL: https://doi.org/10.14711/thesis-b1448978 ; http://repository.ust.hk/ir/bitstream/1783.1-88929/1/th_redirect.html

► Regulatory volume decrease (RVD) is crucial for cells to survive swelling. The volume sensitive outwardly rectifying anion channel (VSOR) is considered to be the major… (more)

▼ Regulatory volume decrease (RVD) is crucial for cells to survive swelling. The volume sensitive outwardly rectifying anion channel (VSOR) is considered to be the major anion channel governing RVD in many tissues and cells. The cystic fibrosis transmembrane conductance regulator (CFTR) functions as both an intracellular ligand-gated channel and a regulator of other channels and transporters in many epithelial tissues. The loss of CFTR impaired RVD of epithelial cells with elusive mechanism. Our lab found that stretch activates CFTR and thus we hypothesize that CFTR may mediate epithelial RVD by directly responding to the mechanical stress induced by cell-swelling. Here we examined the molecular identity of volume-sensing anion channel in epithelia RVD by blocking VSOR and CFTR activities. In Calu-3 cells, an airway epithelial cell-line with highly expressed CFTR, hypotonicity-induced short circuit current (I_sc) is sensitive to CFTR specific inhibitor but not to VSOR inhibitors. The l_sc was independent of cytoplasmic ca²⁺ levels and cAMP levels, suggesting the mechanosensitivity of CFTR played a role. Moreover, genetic suppression or ablation of CFTR markedly reduced swelling induced l_sc. In cultured CHO cells and freshly isolated intestinal crypts expressing CFTR, blocking CFTR abolished RVD triggered by hypotonicity. RVD is important in cell migration. We found that exogenous CFTR expression accelerated cell migration in HEK293T cells. Surprisingly, GSS1D, a CFTR mutation lacking cAMP-induced chloride channel activity, functioned like wild-type CFTR in swelling- or stretch-induced l_sc, RVD and cell migration. Furthermore, cell swelling also activated CFTR in cell-attached membrane patches in Calu-3 cells. Thus, our studies showed that both wild-type and G551D CFTR might be involved in epithelial RVD by responding to the mechanical stress induced by cell-swelling. Our findings also might explain the relative milder phenotype of cystic fibrosis (CF) patients carrying G551D mutation and shed light on developing novel mechanical treatment for CF.

Subjects/Keywords: Cystic fibrosis; Epithelial cells; Cellular control mechanisms

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APA (6^th Edition):

Xie, C. L. (2014). Mechanosensitive gating of CFTR in epithelial cell volume regulation. (Thesis). Hong Kong University of Science and Technology. Retrieved from https://doi.org/10.14711/thesis-b1448978 ; http://repository.ust.hk/ir/bitstream/1783.1-88929/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Xie, Changyan LIFS. “Mechanosensitive gating of CFTR in epithelial cell volume regulation.” 2014. Thesis, Hong Kong University of Science and Technology. Accessed September 15, 2019. https://doi.org/10.14711/thesis-b1448978 ; http://repository.ust.hk/ir/bitstream/1783.1-88929/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Xie, Changyan LIFS. “Mechanosensitive gating of CFTR in epithelial cell volume regulation.” 2014. Web. 15 Sep 2019.

Vancouver:

Xie CL. Mechanosensitive gating of CFTR in epithelial cell volume regulation. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2014. [cited 2019 Sep 15]. Available from: https://doi.org/10.14711/thesis-b1448978 ; http://repository.ust.hk/ir/bitstream/1783.1-88929/1/th_redirect.html.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Xie CL. Mechanosensitive gating of CFTR in epithelial cell volume regulation. [Thesis]. Hong Kong University of Science and Technology; 2014. Available from: https://doi.org/10.14711/thesis-b1448978 ; http://repository.ust.hk/ir/bitstream/1783.1-88929/1/th_redirect.html

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Hong Kong

26. 歐陽鎮怡; Auyeung, Chun-yee, Natalie. Fucosyltransferase-5 on human spermatozoa mediates attachment of spermatozoa to oviductal epithelial cells.

Degree: Master of Medical Sciences, 2008, University of Hong Kong

URL: Auyeung, C. N. [歐陽鎮怡]. (2008). Fucosyltransferase-5 on human spermatozoa mediates attachment of spermatozoa to oviductal epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4073862 ; http://dx.doi.org/10.5353/th_b4073862 ; http://hdl.handle.net/10722/52011

published_or_final_version

Medical Sciences

Master

Master of Medical Sciences

Subjects/Keywords: Fucosyltransferases.; Epithelial cells.

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

歐陽鎮怡; Auyeung, Chun-yee, N. (2008). Fucosyltransferase-5 on human spermatozoa mediates attachment of spermatozoa to oviductal epithelial cells. (Masters Thesis). University of Hong Kong. Retrieved from Auyeung, C. N. [歐陽鎮怡]. (2008). Fucosyltransferase-5 on human spermatozoa mediates attachment of spermatozoa to oviductal epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4073862 ; http://dx.doi.org/10.5353/th_b4073862 ; http://hdl.handle.net/10722/52011

Chicago Manual of Style (16^th Edition):

歐陽鎮怡; Auyeung, Chun-yee, Natalie. “Fucosyltransferase-5 on human spermatozoa mediates attachment of spermatozoa to oviductal epithelial cells.” 2008. Masters Thesis, University of Hong Kong. Accessed September 15, 2019. Auyeung, C. N. [歐陽鎮怡]. (2008). Fucosyltransferase-5 on human spermatozoa mediates attachment of spermatozoa to oviductal epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4073862 ; http://dx.doi.org/10.5353/th_b4073862 ; http://hdl.handle.net/10722/52011.

MLA Handbook (7^th Edition):

歐陽鎮怡; Auyeung, Chun-yee, Natalie. “Fucosyltransferase-5 on human spermatozoa mediates attachment of spermatozoa to oviductal epithelial cells.” 2008. Web. 15 Sep 2019.

Vancouver:

歐陽鎮怡; Auyeung, Chun-yee N. Fucosyltransferase-5 on human spermatozoa mediates attachment of spermatozoa to oviductal epithelial cells. [Internet] [Masters thesis]. University of Hong Kong; 2008. [cited 2019 Sep 15]. Available from: Auyeung, C. N. [歐陽鎮怡]. (2008). Fucosyltransferase-5 on human spermatozoa mediates attachment of spermatozoa to oviductal epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4073862 ; http://dx.doi.org/10.5353/th_b4073862 ; http://hdl.handle.net/10722/52011.

Council of Science Editors:

歐陽鎮怡; Auyeung, Chun-yee N. Fucosyltransferase-5 on human spermatozoa mediates attachment of spermatozoa to oviductal epithelial cells. [Masters Thesis]. University of Hong Kong; 2008. Available from: Auyeung, C. N. [歐陽鎮怡]. (2008). Fucosyltransferase-5 on human spermatozoa mediates attachment of spermatozoa to oviductal epithelial cells. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4073862 ; http://dx.doi.org/10.5353/th_b4073862 ; http://hdl.handle.net/10722/52011

University of Hong Kong

27. 何秀鈞; Ho, Sau-kwan. Interactions of anti-dsDNA antibodies with human proximal renal tubular epithelial cells in the pathogenesis of lupus nephritis.

Degree: M. Phil., 2013, University of Hong Kong

URL: Ho, S. [何秀鈞]. (2013). Interactions of anti-dsDNA antibodies with human proximal renal tubular epithelial cells in the pathogenesis of lupus nephritis. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5053361 ; http://dx.doi.org/10.5353/th_b5053361 ; http://hdl.handle.net/10722/197161

► Lupus nephritis is characterized by the production of anti-dsDNA antibodies, deposition of immune complexes within the kidney parenchyma, proliferation of resident renal cells and induction… (more)

▼ Lupus nephritis is characterized by the production of anti-dsDNA antibodies, deposition of immune complexes within the kidney parenchyma, proliferation of resident renal cells and induction of inflammatory and fibrotic processes. Approximately 70% of patients with lupus nephritis show immune aggregates along the tubular basement membrane, which is accompanied by an influx of infiltrating cells and increased intra-renal expression of IL-6. Much attention has focused on the inflammatory processes in the kidney during pathogenesis of lupus nephritis whereas mechanisms of fibrogenesis are less well characterized. Tubulo-interstitial injury is a key indicator of poor prognosis of renal function. Given that the tubulo-interstitium occupies over 80% of the kidney volume, injury to this compartment will have a major impact on renal function. There is evidence to show that proximal tubular epithelial cells (PTEC) undergo epithelial-to-mesenchymal transition (EMT) during pathological disorders and adopt a fibroblastic morphology with increased fibrogenic potential. We have previously demonstrated that anti-dsDNA antibodies bound directly to the surface of PTEC through cross-reactive proteins, which were subsequently internalized and translocated to the nucleus where they induced functional changes. Using a proteomic approach, this study identified the cross-reactive antigens that mediated anti-dsDNA antibody binding and intracellular localization in PTEC and the functional consequences thereafter, focusing on EMT and fibrogenic events. Human polyclonal anti-dsDNA antibodies isolated from patients with lupus nephritis bound to Ku70 in plasma membrane extracts isolated from PTEC, and to Ku70, Ku80 and major vault protein in cytosolic and nuclear fractions. Anti-dsDNA antibodies increased synthesis of Ku70, Ku80 and major vault protein in PTEC in a time-dependent manner. Expression of these proteins was localized to proximal tubules especially those undergoing atrophy, and staining was more prominent in renal biopsies from patients with lupus nephritis compared to non-lupus renal disease or control specimens. Binding of anti-dsDNA antibodies to PTEC increased phosphorylation of MAPK and PKC signaling pathways that was accompanied by a concomitant increase in IL-6, IL-8 and TGF-1 secretion and synthesis of β-catenin, fibroblast specific protein-1, fibronectin and laminin. Inhibition of MAPK and PKC signaling pathways with specific inhibitors revealed differential regulation of inflammatory and fibrotic processes by these signaling pathways. In this respect, increased ERK, p38 MAPK, JNK and PKC phosphorylation in PTEC following anti-dsDNA antibody stimulation enhanced IL-6, IL-8 and fibronectin synthesis, whereas increased ERK and JNK phosphorylation upregulated TGF-β1 secretion. Increased β-catenin synthesis was mediated through JNK and PKC phosphorylation. Taken together, our data suggest that PTEC contribute to the pathogenesis of renal inflammation and fibrosis in lupus nephritis. We hypothesize that anti-dsDNA…

Subjects/Keywords: Epithelial cells; Lupus nephritis - Pathogenesis; DNA antibodies

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

何秀鈞; Ho, S. (2013). Interactions of anti-dsDNA antibodies with human proximal renal tubular epithelial cells in the pathogenesis of lupus nephritis. (Masters Thesis). University of Hong Kong. Retrieved from Ho, S. [何秀鈞]. (2013). Interactions of anti-dsDNA antibodies with human proximal renal tubular epithelial cells in the pathogenesis of lupus nephritis. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5053361 ; http://dx.doi.org/10.5353/th_b5053361 ; http://hdl.handle.net/10722/197161

Chicago Manual of Style (16^th Edition):

何秀鈞; Ho, Sau-kwan. “Interactions of anti-dsDNA antibodies with human proximal renal tubular epithelial cells in the pathogenesis of lupus nephritis.” 2013. Masters Thesis, University of Hong Kong. Accessed September 15, 2019. Ho, S. [何秀鈞]. (2013). Interactions of anti-dsDNA antibodies with human proximal renal tubular epithelial cells in the pathogenesis of lupus nephritis. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5053361 ; http://dx.doi.org/10.5353/th_b5053361 ; http://hdl.handle.net/10722/197161.

MLA Handbook (7^th Edition):

何秀鈞; Ho, Sau-kwan. “Interactions of anti-dsDNA antibodies with human proximal renal tubular epithelial cells in the pathogenesis of lupus nephritis.” 2013. Web. 15 Sep 2019.

Vancouver:

何秀鈞; Ho S. Interactions of anti-dsDNA antibodies with human proximal renal tubular epithelial cells in the pathogenesis of lupus nephritis. [Internet] [Masters thesis]. University of Hong Kong; 2013. [cited 2019 Sep 15]. Available from: Ho, S. [何秀鈞]. (2013). Interactions of anti-dsDNA antibodies with human proximal renal tubular epithelial cells in the pathogenesis of lupus nephritis. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5053361 ; http://dx.doi.org/10.5353/th_b5053361 ; http://hdl.handle.net/10722/197161.

Council of Science Editors:

何秀鈞; Ho S. Interactions of anti-dsDNA antibodies with human proximal renal tubular epithelial cells in the pathogenesis of lupus nephritis. [Masters Thesis]. University of Hong Kong; 2013. Available from: Ho, S. [何秀鈞]. (2013). Interactions of anti-dsDNA antibodies with human proximal renal tubular epithelial cells in the pathogenesis of lupus nephritis. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b5053361 ; http://dx.doi.org/10.5353/th_b5053361 ; http://hdl.handle.net/10722/197161

28. Moreno Layseca, Paulina. The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia.

Degree: PhD, 2015, University of Manchester

URL: https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-1integrin-in-normal-and-oncogenemediated-proliferation-in-breast-epithelia(635388a7-5382-4cb5-82d1-d098b2092e2e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.634970

► Luminal epithelial cells in the mammary gland require two types of signals to proliferate: soluble signals (growth factor signals) and signals from the extracellular matrix… (more)

▼ Luminal epithelial cells in the mammary gland require two types of signals to proliferate: soluble signals (growth factor signals) and signals from the extracellular matrix (ECM). The composition of the ECM is sensed by adhesion receptors such as integrins. Integrins modulate cell behaviour and play a key role in cell cycle entry. Altered integrin expression and signalling has been associated with breast cancer and studies using mouse mammary epithelial cells (MECs) have shown that the absence of β1-integrin induces growth arrest. However, it is not completely understood how integrins transduce the signals from the plasma membrane to the nucleus to induce cell cycle entry. Thus, the first aim of this project was to determine how β1-integrin controls proliferation in MECs. I established a model to study the effects of depleting β1-integrin using the FSK7 mammary epithelial cell line. The proliferation defect observed in this β1-integrin knockdown model was rescued by expressing a constitutively active Rac1 or Pak. Moreover, inhibiting Rac1 or Pak prevented normal proliferation in MECs in a similar fashion as β1-integrin depletion. Furthermore, in this thesis I have identified the complex comprised of Src, paxillin and p130Cas as a potential link between β1-integrin and Rac1. These results provide an insight into the mechanism that regulates proliferation downstream of β1-integrin. During breast cancer initiation, β1-integrin signals are disrupted. This indicates that additional signals must be driving proliferation during tumorigenesis. Therefore, the second aim of this project was to test whether expression of breast oncogenes can overcome the proliferation defect present in β1-integrin null cells. In order to do so, an oncogenic ErbB2, a constitutively active form of Akt (myrAkt) and the Notch1 intracellular domain (NICD) were transfected in the β1-integrin knockdown MECs. The results showed that ErbB2 overcomes the need for β1-integrin by signalling to Pak. NICD does not require β1-integrin to drive proliferation by an unknown mechanism. Expression of myrAkt did not restore normal levels of proliferation in β1-integrin depleted MECs. This finding suggests that Akt is not sufficient to induce cell cycle entry by itself and instead, both Akt and Erk signalling are needed to exert this function. This work has further delineated the specific signals controlling proliferation downstream of β1-integrin, and has provided a model to test the dependence of oncogenes for β1-integrin to drive proliferation in MECs. These studies are important to understand the role of β1-integrin in breast cancer formation and to define the types of breast cancer where β1-integrin can be used as an effective therapeutic target.

Subjects/Keywords: 611; Integrins; Proliferation; Mammary epithelial cells

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APA (6^th Edition):

Moreno Layseca, P. (2015). The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-1integrin-in-normal-and-oncogenemediated-proliferation-in-breast-epithelia(635388a7-5382-4cb5-82d1-d098b2092e2e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.634970

Chicago Manual of Style (16^th Edition):

Moreno Layseca, Paulina. “The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia.” 2015. Doctoral Dissertation, University of Manchester. Accessed September 15, 2019. https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-1integrin-in-normal-and-oncogenemediated-proliferation-in-breast-epithelia(635388a7-5382-4cb5-82d1-d098b2092e2e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.634970.

MLA Handbook (7^th Edition):

Moreno Layseca, Paulina. “The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia.” 2015. Web. 15 Sep 2019.

Vancouver:

Moreno Layseca P. The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia. [Internet] [Doctoral dissertation]. University of Manchester; 2015. [cited 2019 Sep 15]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-1integrin-in-normal-and-oncogenemediated-proliferation-in-breast-epithelia(635388a7-5382-4cb5-82d1-d098b2092e2e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.634970.

Council of Science Editors:

Moreno Layseca P. The role of β1-integrin in normal and oncogene-mediated proliferation in breast epithelia. [Doctoral Dissertation]. University of Manchester; 2015. Available from: https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-1integrin-in-normal-and-oncogenemediated-proliferation-in-breast-epithelia(635388a7-5382-4cb5-82d1-d098b2092e2e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.634970

Cornell University

29. Ju, Chia-Hsin. Innate Immunity Of The Intestinal Epithelium During Toxoplasma Gondii Infection .

Degree: 2011, Cornell University

URL: http://hdl.handle.net/1813/33498

► The single layer of epithelial cells that line the intestinal tract provides both a physiologic and immunologic barrier for microbes and foreign antigens. Intestinal epithelial… (more)

▼ The single layer of epithelial cells that line the intestinal tract provides both a physiologic and immunologic barrier for microbes and foreign antigens. Intestinal epithelial cells are differentiated into different functional subtypes and have regulatory roles in maintaining the homeostasis of the gut as well as initiating inflammatory responses during pathogenic infections. Toxoplasma gondii is a widespread zoonotic protozoan parasite that infects warm-blooded animals. Infection usually occurs through ingestion of T. gondii contaminated food or water. Therefore, natural route of infection has revealed the importance of epithelial cell response in influencing the outcome of the local and systemic immune response. In this thesis, I examined the innate immune response of intestinal epithelial cell during T. gondii infection. The immediate response upon intestinal epithelial and parasite contact revealed that T. gondii infected epithelial cells elicited MAPK phosphorylation, NF-!B activation, and secretion of IL-8 as well as several other inflammatory cytokines and chemokines in epithelial cells. I found that activation of MAPK and production of IL-8 was dependent on the MyD88 signaling pathway, and TLR2 was sufficient for parasite induced signaling in HEK 293 transfected cells. In addition, TLR2 signaling plays an important role in modulating of the local intestinal environment by inducing migration of dendritic cells into the follicle-associated epithelium of Peyer's patches. Using the susceptible C57BL/6 mice as a model, morphological changes of different intestinal epithelial cell subtypes in response to peroral T. gondii infection were further characterized. Oral infection with T. gondii ME49 cysts induced intestinal pathology and morphological changes of different epithelial cell subtypes. Mice deficient in TLR2 were more resistant to intestinal pathology and associated morphological changes. Parasite-derived TLR2 stimulatory molecules were found to be present in the supernatant collected from T. gondii infected cells. Therefore, potential biological significance of the activity in supernatants from T. gondii infected cells was also investigated. I found that the supernatants from T. gondii infected cells enhanced luminal antigen uptake and induced TLR2-dependent migration of dendritic cells to the follicle associated epithelium of Peyer's patches. Furthermore, analysis of the supernatant revealed several T. gondii proteins, and the GPI-anchored surface antigen-1 contributes to TLR2 stimulatory activity. In summary, this dissertation explores the innate immune response of the intestinal epithelium during T. gondii infection. The signaling pathways of intestinal epithelial cells elicited by the parasite as well as the modulation of the local intestinal environment can help us better understand the immunopathogenesis of T. gondii infection. Advisors/Committee Members: Denkers, Eric Young (committeeMember), Marquis, Helene (committeeMember), Clark, Theodore G. (committeeMember).

Subjects/Keywords: Innate immunity; Intestinal epithelial cells; Toxoplasma gondii

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APA (6^th Edition):

Ju, C. (2011). Innate Immunity Of The Intestinal Epithelium During Toxoplasma Gondii Infection . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/33498

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ju, Chia-Hsin. “Innate Immunity Of The Intestinal Epithelium During Toxoplasma Gondii Infection .” 2011. Thesis, Cornell University. Accessed September 15, 2019. http://hdl.handle.net/1813/33498.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ju, Chia-Hsin. “Innate Immunity Of The Intestinal Epithelium During Toxoplasma Gondii Infection .” 2011. Web. 15 Sep 2019.

Vancouver:

Ju C. Innate Immunity Of The Intestinal Epithelium During Toxoplasma Gondii Infection . [Internet] [Thesis]. Cornell University; 2011. [cited 2019 Sep 15]. Available from: http://hdl.handle.net/1813/33498.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ju C. Innate Immunity Of The Intestinal Epithelium During Toxoplasma Gondii Infection . [Thesis]. Cornell University; 2011. Available from: http://hdl.handle.net/1813/33498

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of California – Merced

30. Sater, Ali Abbas Abdul. Chlamydia induced caspase-1 activation is inflammasome dependent: role and sources of reactive oxygen species in chlamydial growth.

Degree: Quantitative and Systems Biology, 2010, University of California – Merced

URL: http://www.escholarship.org/uc/item/6jr544w6

► Inflammasomes have been extensively characterized in monocytes and macrophages, but not in epithelial cells, which are the preferred host cells for many pathogens. Here we… (more)

Subjects/Keywords: Biology.; Chlamydia.; Epithelial cells.; Caspase-1.

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sater, A. A. A. (2010). Chlamydia induced caspase-1 activation is inflammasome dependent: role and sources of reactive oxygen species in chlamydial growth. (Thesis). University of California – Merced. Retrieved from http://www.escholarship.org/uc/item/6jr544w6

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Sater, Ali Abbas Abdul. “Chlamydia induced caspase-1 activation is inflammasome dependent: role and sources of reactive oxygen species in chlamydial growth.” 2010. Thesis, University of California – Merced. Accessed September 15, 2019. http://www.escholarship.org/uc/item/6jr544w6.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Sater, Ali Abbas Abdul. “Chlamydia induced caspase-1 activation is inflammasome dependent: role and sources of reactive oxygen species in chlamydial growth.” 2010. Web. 15 Sep 2019.

Vancouver:

Sater AAA. Chlamydia induced caspase-1 activation is inflammasome dependent: role and sources of reactive oxygen species in chlamydial growth. [Internet] [Thesis]. University of California – Merced; 2010. [cited 2019 Sep 15]. Available from: http://www.escholarship.org/uc/item/6jr544w6.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Sater AAA. Chlamydia induced caspase-1 activation is inflammasome dependent: role and sources of reactive oxygen species in chlamydial growth. [Thesis]. University of California – Merced; 2010. Available from: http://www.escholarship.org/uc/item/6jr544w6

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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