+publisher:"Georgia Tech" +contributor:("Jo, Hanjoong")

1. Salim, Md Tausif Tausif. Role of microRNA 214 in cyclic stretch induced aortic valve pathogenesis.

Degree: MS, Chemical and Biomolecular Engineering, 2018, Georgia Tech

► Calcific aortic valve disease (CAVD) is one of the most prevalent valvular diseases among the elderly population. Unfortunately, there are no therapeutic drugs available to… (more)

Subjects/Keywords: Aortic valve; miR-214; Cyclic stretch

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APA (6^th Edition):

Salim, M. T. T. (2018). Role of microRNA 214 in cyclic stretch induced aortic valve pathogenesis. (Masters Thesis). Georgia Tech. Retrieved from http://hdl.handle.net/1853/61174

Chicago Manual of Style (16^th Edition):

Salim, Md Tausif Tausif. “Role of microRNA 214 in cyclic stretch induced aortic valve pathogenesis.” 2018. Masters Thesis, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/61174.

MLA Handbook (7^th Edition):

Salim, Md Tausif Tausif. “Role of microRNA 214 in cyclic stretch induced aortic valve pathogenesis.” 2018. Web. 16 Apr 2021.

Vancouver:

Salim MTT. Role of microRNA 214 in cyclic stretch induced aortic valve pathogenesis. [Internet] [Masters thesis]. Georgia Tech; 2018. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/61174.

Council of Science Editors:

Salim MTT. Role of microRNA 214 in cyclic stretch induced aortic valve pathogenesis. [Masters Thesis]. Georgia Tech; 2018. Available from: http://hdl.handle.net/1853/61174

Georgia Tech

2. Sei, Yoshitaka John. Microfluidics for translating multifunctional nanomaterials.

Degree: PhD, Mechanical Engineering, 2018, Georgia Tech

URL: http://hdl.handle.net/1853/62187

► Conflicting results between benchtop experiments, animal models, and clinical trials have posed a significant challenge in translational medical research, motivating the development of technologies with… (more)

▼ Conflicting results between benchtop experiments, animal models, and clinical trials have posed a significant challenge in translational medical research, motivating the development of technologies with which to assess and screen experimental therapeutics. Among these new technologies are microfluidic platforms that allow for the synthesis of nanoparticles and the tuning of microenvironments to replicate the ideal physiological conditions to study living responses in vitro. The advantages of using microfluidic technologies in order to accomplish these feats are attributed to volumetrically minimal usage of expensive reagents while also having the capacity to be run continuously for high-throughput and large-scale applications. Some of the challenges still associated to the general adoption of microfluidic technologies are those typically found in the early stages of new technological advancements: (1) a lack of standardization in work flow and platform design, and (2) a limited accessibility to specialized equipment. This thesis focuses on contributing to the standardization of the microfluidic workflow through exploring both platform designs for the synthesis and screening of nanoparticles, and exploring key translational questions with experiments that are uniquely enabled with microfluidics. The microfluidic platforms that are presented in this work are a mixer for nanoparticle synthesis and a monitor for the permeability of a cellular monolayer. These platforms were implemented in experiments studying the functionality of high-density lipoprotein mimetic nanoparticles and their interactions with endothelial cells within the context of cardiovascular disease. We report how the functionality of the high-density lipoprotein mimetic nanoparticles is affected by its protein composition, and how its interactions with the endothelial monolayer are modulated depending on the oscillatory flow stimulated inflammatory condition of the endothelial cells. Advisors/Committee Members: Kim, YongTae (advisor), Champion, Julie (committee member), Dixon, James B. (committee member), García, Andrés (committee member), Jo, Hanjoong (committee member).

Subjects/Keywords: Microfluidics; Nanomaterials

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APA (6^th Edition):

Sei, Y. J. (2018). Microfluidics for translating multifunctional nanomaterials. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/62187

Chicago Manual of Style (16^th Edition):

Sei, Yoshitaka John. “Microfluidics for translating multifunctional nanomaterials.” 2018. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/62187.

MLA Handbook (7^th Edition):

Sei, Yoshitaka John. “Microfluidics for translating multifunctional nanomaterials.” 2018. Web. 16 Apr 2021.

Vancouver:

Sei YJ. Microfluidics for translating multifunctional nanomaterials. [Internet] [Doctoral dissertation]. Georgia Tech; 2018. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/62187.

Council of Science Editors:

Sei YJ. Microfluidics for translating multifunctional nanomaterials. [Doctoral Dissertation]. Georgia Tech; 2018. Available from: http://hdl.handle.net/1853/62187

Georgia Tech

3. Gray, Warren Dale. Development of therapeutic systems to treat the infarcted heart.

Degree: PhD, Biomedical Engineering (Joint GT/Emory Department), 2014, Georgia Tech

URL: http://hdl.handle.net/1853/53429

► Cardiovascular disease is the leading cause of morbidity and mortality in developed nations, and heart disease is predicted to remain the leading killer for the… (more)

Subjects/Keywords: Myocardial infarction; Cardiac protection; Cardiac regeneration; Angiogenesis; Therapeutic system; Nanoparticle; Dendrimer; Exosome; Hypoxia; N-acetylglucosamine

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APA (6^th Edition):

Gray, W. D. (2014). Development of therapeutic systems to treat the infarcted heart. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/53429

Chicago Manual of Style (16^th Edition):

Gray, Warren Dale. “Development of therapeutic systems to treat the infarcted heart.” 2014. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/53429.

MLA Handbook (7^th Edition):

Gray, Warren Dale. “Development of therapeutic systems to treat the infarcted heart.” 2014. Web. 16 Apr 2021.

Vancouver:

Gray WD. Development of therapeutic systems to treat the infarcted heart. [Internet] [Doctoral dissertation]. Georgia Tech; 2014. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/53429.

Council of Science Editors:

Gray WD. Development of therapeutic systems to treat the infarcted heart. [Doctoral Dissertation]. Georgia Tech; 2014. Available from: http://hdl.handle.net/1853/53429

Georgia Tech

4. Rathan, Swetha. Aortic valve mechanobiology- role of altered hemodynamics in mediating aortic valve inflammation and calcification.

Degree: PhD, Chemical and Biomolecular Engineering, 2016, Georgia Tech

URL: http://hdl.handle.net/1853/58144

► Calcific aortic valve (AV) disease is a strong risk factor for cardiovascular related deaths and is a significant source of mortality worldwide, with the number… (more)

▼ Calcific aortic valve (AV) disease is a strong risk factor for cardiovascular related deaths and is a significant source of mortality worldwide, with the number of patients requiring AV surgery expected to increase from 250,000 to 850,000 by 2050. However, the molecular mechanisms underlying AV disease have not been well studied or understood. Further, identification of biomarkers that can be used to detect early stage AV disease is also understudied but vital to successfully preventing and/or treating AV disease. It was hypothesized that sclerosis, inflammation and calcification preferentially occurs in the fibrosa compared to the ventricularis due to differential gene expression and oscillatory shear stress. Freshly isolated porcine AV leaflets and an ex vivo shear stress bioreactor was used to test this hypothesis. The low magnitude oscillatory shear stress (OS) appeared to predispose fibrosa to side-dependent calcification via increasing collagen turnover (Col1a1), and thickening of the extracellular matrix (ECM) (fibrosis) and decreasing the expression of genes that protect endothelial function (Klf4 and Enos). The unidirectional pulsatile shear, LS, however, preserved the ECM and gene expression in the ventricularis. The involvement of miRNAs in OS mediated AV pathogenesis was also investigated in a shear- and side-dependent manner. The miR-214 was found to play a role in this OS induced pathogenesis in fibrosa but not ventricularis. Using an ex vivo miRNA silencing protocol, anti-miRNA was delivered to both endothelial and interstitial cells of the AV tissue without compromising the cell viability. Silencing of miR-214 showed that the OS induced pathology in the fibrosa is likely to be mediated via miR-214, klf4 and Tgfβ1 dependent pathway that can lead to AV fibrosis, endothelial-to-mesenchymal transition and eventually sclerosis. The miR-214, however, did not play a role in shear-induced inflammation and calcification. The miR-214, as such, is likely to play a key role in the early onset of side- and shear- dependent AV disease and has a potential to serve as a disease biomarker. Further, an ex vivo AV calcification model was also developed to understand the role of endogenous pro- and anti-calcification factors, such as inorganic pyrophosphate, orthophosphate, and alkaline phosphatase. The functional studies carried out in this dissertation aim to link the mechanosensitive miRNAs to the genes involved in inflammation, endothelial-to-mesenchymal transition, and cell apoptosis etc, which eventually causes AV leaflets to calcify. Thus improved understanding of AV disease mechanisms under different hemodynamic conditions will enable us to improve the design of tissue-engineered valves and develop non-surgical treatment options. Advisors/Committee Members: Yoganathan, Ajit P. (advisor), Jo, Hanjoong (committee member), Taylor, W. Robert (committee member), Champion, Julie A. (committee member), Nerem, Robert M. (committee member).

Subjects/Keywords: Aortic valve; Hemodynamics; Mechanobiology; MicroRNA; Calcification

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APA (6^th Edition):

Rathan, S. (2016). Aortic valve mechanobiology- role of altered hemodynamics in mediating aortic valve inflammation and calcification. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/58144

Chicago Manual of Style (16^th Edition):

Rathan, Swetha. “Aortic valve mechanobiology- role of altered hemodynamics in mediating aortic valve inflammation and calcification.” 2016. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/58144.

MLA Handbook (7^th Edition):

Rathan, Swetha. “Aortic valve mechanobiology- role of altered hemodynamics in mediating aortic valve inflammation and calcification.” 2016. Web. 16 Apr 2021.

Vancouver:

Rathan S. Aortic valve mechanobiology- role of altered hemodynamics in mediating aortic valve inflammation and calcification. [Internet] [Doctoral dissertation]. Georgia Tech; 2016. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/58144.

Council of Science Editors:

Rathan S. Aortic valve mechanobiology- role of altered hemodynamics in mediating aortic valve inflammation and calcification. [Doctoral Dissertation]. Georgia Tech; 2016. Available from: http://hdl.handle.net/1853/58144

Georgia Tech

5. Caesar, Christa. The role and regulation of osteopontin in hypertension related remodeling and inflammation of the aorta.

Degree: PhD, Biomedical Engineering (Joint GT/Emory Department), 2016, Georgia Tech

URL: http://hdl.handle.net/1853/58157

► The arterial wall experiences elevated mechanical strain in the setting of hypertension, which leads to vascular inflammation and atherosclerosis. However, many of the underlying molecular… (more)

Subjects/Keywords: Osteopontin; Hypertension; Aorta; Mechanical strain; Hydrogen peroxide

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APA (6^th Edition):

Caesar, C. (2016). The role and regulation of osteopontin in hypertension related remodeling and inflammation of the aorta. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/58157

Chicago Manual of Style (16^th Edition):

Caesar, Christa. “The role and regulation of osteopontin in hypertension related remodeling and inflammation of the aorta.” 2016. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/58157.

MLA Handbook (7^th Edition):

Caesar, Christa. “The role and regulation of osteopontin in hypertension related remodeling and inflammation of the aorta.” 2016. Web. 16 Apr 2021.

Vancouver:

Caesar C. The role and regulation of osteopontin in hypertension related remodeling and inflammation of the aorta. [Internet] [Doctoral dissertation]. Georgia Tech; 2016. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/58157.

Council of Science Editors:

Caesar C. The role and regulation of osteopontin in hypertension related remodeling and inflammation of the aorta. [Doctoral Dissertation]. Georgia Tech; 2016. Available from: http://hdl.handle.net/1853/58157

Georgia Tech

6. Wen, Mary Mei. New strategies for tagging quantum dots for dynamic cellular imaging.

Degree: PhD, Biomedical Engineering (Joint GT/Emory Department), 2013, Georgia Tech

URL: http://hdl.handle.net/1853/52150

► In recent years, semiconductor quantum dots (QDs) have arisen as a new class of fluorescent probes that possess unique optical and electronic properties well-suited for… (more)

▼ In recent years, semiconductor quantum dots (QDs) have arisen as a new class of fluorescent probes that possess unique optical and electronic properties well-suited for single-molecule imaging of dynamic live cell processes. Nonetheless, the large size of conventional QD-ligand constructs has precluded their widespread use in single-molecule studies, especially on cell interiors. A typical QD-ligand construct can range upwards of 35 nm in diameter, well exceeding the size threshold for cytosolic diffusion and posing steric hindrance to binding cell receptors. The objective of this research is to develop tagging strategies that allow QD-ligand conjugates to specifically bind their target proteins while maintaining a small overall construct size. To achieve this objective, we utilize the HaloTag protein (HTP) available from Promega Corporation, which reacts readily with a HaloTag ligand (HTL) to form a covalent bond. When HaloTag ligands are conjugated to size-minimized multidentate polymer coated QDs, compact QD-ligand constructs less than 15 nm in diameter can be produced. These quantum dot-HaloTag ligand (QD-HTL) conjugates can then be used to covalently bind and track cellular receptors genetically fused to the HaloTag protein. In this study, size-minimized quantum dot-HaloTag ligand conjugates are synthesized and evaluated for their ability to bind specifically to purified and cellular HTP. The effect of QD-HTL surface modifications on different types of specific and nonspecific cellular binding are systematically investigated. Finally, these QD-HTL conjugates are utilized for single-molecule imaging of dynamic live cell processes. Our results show that size-minimized QD-HTLs exhibit great promise as novel imaging probes for live cell imaging, allowing researchers to visualize cellular protein dynamics in remarkable detail. Advisors/Committee Members: Nie, Shuming (advisor), Bao, Gang (committee member), Jo, Hanjoong (committee member), Merrill, Alfred (committee member), Santangelo, Philip (committee member).

Subjects/Keywords: Quantum dots; Live cell imaging; Single molecule imaging; HaloTag; Tagging strategies; Nanotechnology; Bionanotechnology

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APA (6^th Edition):

Wen, M. M. (2013). New strategies for tagging quantum dots for dynamic cellular imaging. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/52150

Chicago Manual of Style (16^th Edition):

Wen, Mary Mei. “New strategies for tagging quantum dots for dynamic cellular imaging.” 2013. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/52150.

MLA Handbook (7^th Edition):

Wen, Mary Mei. “New strategies for tagging quantum dots for dynamic cellular imaging.” 2013. Web. 16 Apr 2021.

Vancouver:

Wen MM. New strategies for tagging quantum dots for dynamic cellular imaging. [Internet] [Doctoral dissertation]. Georgia Tech; 2013. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/52150.

Council of Science Editors:

Wen MM. New strategies for tagging quantum dots for dynamic cellular imaging. [Doctoral Dissertation]. Georgia Tech; 2013. Available from: http://hdl.handle.net/1853/52150

Georgia Tech

7. Keegan, Philip Michael. Shear stress, hemodynamics, and proteolytic mechanisms underlying large artery remodeling in sickle cell disease.

Degree: PhD, Biomedical Engineering (Joint GT/Emory Department), 2014, Georgia Tech

URL: http://hdl.handle.net/1853/54289

► Sickle cell disease is a genetic disorder that affects 100,000 Americans and millions more worldwide. Although the sickle mutation affects one protein, which is only… (more)

▼ Sickle cell disease is a genetic disorder that affects 100,000 Americans and millions more worldwide. Although the sickle mutation affects one protein, which is only expressed in a single cell type, it has profound detrimental effects on nearly every organ system in the body. Young children with sickle cell disease have an 11% chance of suffering a major stroke event by the age of 16, and a 35% chance of developing ÒsilentÓ strokes that often result in significant learning and mental disabilities. Clinical investigations suggest that stroke development in people with sickle cell disease results from luminal narrowing of the carotid and cerebral arteries due to excess matrix deposition and fragmentation of the elastic lamina; however, the underlying cellular mechanisms that initiate arterial remodeling in sickle cell disease remain relatively unknown. Cathepsins K and V are members of the cysteine family of proteases and represent two of the most potent elastases yet identified in humans. Furthermore, the role of Cathepsins has been well established in other cardiovascular remodeling diseases, such as atherosclerosis. Due to the compelling histological similarities between vasculopathy in sickle cell disease and atherosclerosis, we tested the hypothesis that the unique inflammatory milieu, in conjunction with the biomechanical vascular environment of sickle cell disease upregulates cathepsin K and V activity in large artery endothelial cells, ultimately leading to arterial remodeling and stroke. Currently, there are few therapeutic options for the prevention of stroke in sickle cell disease; those that do exist carry significant health risks and side effects. Together, this body of work has generated a more mechanistic understanding of how the sickle milieu stimulates the endothelium to initiate arterial remodeling, which has enabled us to identify important pathways (JNK, NFκB) downstream of inflammatory and biomechanical stimuli and validate new therapeutic targets within the JNK pathway to establish preclinical proof of efficacy for the prevention of arterial remodeling in sickle cell disease. Advisors/Committee Members: Platt, Manu O. (advisor), Giddens, Don (committee member), Pace, Betty (committee member), Jo, Hanjoong (committee member), Joiner, Clinton (committee member).

Subjects/Keywords: Sickle cell disease; Arterial remodeling; Cathepsins; Stroke; Hemodynamics; Shear stress

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APA (6^th Edition):

Keegan, P. M. (2014). Shear stress, hemodynamics, and proteolytic mechanisms underlying large artery remodeling in sickle cell disease. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/54289

Chicago Manual of Style (16^th Edition):

Keegan, Philip Michael. “Shear stress, hemodynamics, and proteolytic mechanisms underlying large artery remodeling in sickle cell disease.” 2014. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/54289.

MLA Handbook (7^th Edition):

Keegan, Philip Michael. “Shear stress, hemodynamics, and proteolytic mechanisms underlying large artery remodeling in sickle cell disease.” 2014. Web. 16 Apr 2021.

Vancouver:

Keegan PM. Shear stress, hemodynamics, and proteolytic mechanisms underlying large artery remodeling in sickle cell disease. [Internet] [Doctoral dissertation]. Georgia Tech; 2014. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/54289.

Council of Science Editors:

Keegan PM. Shear stress, hemodynamics, and proteolytic mechanisms underlying large artery remodeling in sickle cell disease. [Doctoral Dissertation]. Georgia Tech; 2014. Available from: http://hdl.handle.net/1853/54289

8. Balderrama, Fanor Alberto. Incorporation of recombinant fibronectin into genetically engineered elastin-based polymers.

Degree: MS, Bioengineering, 2009, Georgia Tech

URL: http://hdl.handle.net/1853/31640

► Cardiovascular disease is the main cause of death in the United States. Many of these conditions require the grafting or bypassing of compromised blood vessels.… (more)

Subjects/Keywords: Functionalization; Coating; Protein; Crosslinking; Genipin; HUVEC; Stability; Cell proliferation; Vascular graft; Elastin; FNIII7-10; Cell adhesion; Endothelialization; Endothelial; Fibronectins; Globulins; Biomedical materials; Vascular grafts

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APA (6^th Edition):

Balderrama, F. A. (2009). Incorporation of recombinant fibronectin into genetically engineered elastin-based polymers. (Masters Thesis). Georgia Tech. Retrieved from http://hdl.handle.net/1853/31640

Chicago Manual of Style (16^th Edition):

Balderrama, Fanor Alberto. “Incorporation of recombinant fibronectin into genetically engineered elastin-based polymers.” 2009. Masters Thesis, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/31640.

MLA Handbook (7^th Edition):

Balderrama, Fanor Alberto. “Incorporation of recombinant fibronectin into genetically engineered elastin-based polymers.” 2009. Web. 16 Apr 2021.

Vancouver:

Balderrama FA. Incorporation of recombinant fibronectin into genetically engineered elastin-based polymers. [Internet] [Masters thesis]. Georgia Tech; 2009. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/31640.

Council of Science Editors:

Balderrama FA. Incorporation of recombinant fibronectin into genetically engineered elastin-based polymers. [Masters Thesis]. Georgia Tech; 2009. Available from: http://hdl.handle.net/1853/31640

Georgia Tech

9. Fernandez Esmerats, Joan. The role of flow-sensitive MiRNAs and UBE2C-dependent HIF1α pathway in calcific aortic valve disease.

Degree: PhD, Biomedical Engineering (Joint GT/Emory Department), 2018, Georgia Tech

URL: http://hdl.handle.net/1853/62206

► Calcific Aortic Valve Disease (CAVD), characterized by aortic valve (AV) stenosis and insufficiency (regurgitation), is a major cause of cardiac-related deaths worldwide, especially in the… (more)

▼ Calcific Aortic Valve Disease (CAVD), characterized by aortic valve (AV) stenosis and insufficiency (regurgitation), is a major cause of cardiac-related deaths worldwide, especially in the aging population in advanced countries. Once developed, it is treated mainly with AV repair or replacement by surgical or transcathether methods; however, there are currently no pharmacological treatment options for these patients. This is largely due to a relative paucity in molecular mechanistic understanding of the disease. CAVD was once thought to be a passive degenerative disease, but overwhelming evidence demonstrates that it is actively regulated by cellular and molecular pathways that lead to AV inflammation, sclerosis (thickening and fibrosis), and calcific lesions. MicroRNAs (miRNAs) are a large class of evolutionarily conserved, noncoding RNAs which function as post-transcriptional regulators by interacting with the 3’ untranslated region (3’UTR) of specific target mRNAs in a sequence-specific manner. A single miRNA can typically target hundreds of mRNAs. These miRNAs negatively regulate gene expression through translational repression or mRNA cleavage, depending on the degree of complementarity. Flow-sensitive miRNAs have been mostly characterized in vitro however, their role in human disease has not been fully studied. Previous work in our laboratory has focused on identifying shear-sensitive and side-specific (ventricularis compared to fibrosa layers of the AV) miRNAs relevant to CAVD. To this end, we conducted two independent microRNA array studies. First, we isolated human aortic valve endothelial cells (HAVECs) from each side of the leaflet and exposed them to high-magnitude unidirectional laminar shear stress (LS) or low-magnitude oscillatory shear stress (OS) conditions for 24 hours to discover shear-sensitive miRNAs. Second, we isolated endothelial-enriched total RNAs from each side of the leaflet from porcine AVs to discover side-specific miRNAs. These studies allowed us to identify miR-181b and miR-483 as potential miRNAs for further studies. In Aim 1, we focused on studying shear-sensitive miR-181b. We showed that miR-181b was upregulated in OS conditions and that it regulates matrix metalloproteinases (MMP) activity in valvular endothelium. We conducted an in silico analysis combining predicted gene targets of miR-181b and shear-sensitive target genes from our in vitro HAVEC array and identified tissue inhibitor of metalloproteinases 3 (TIMP3) as a shear-sensitive target of miR-181b responsible for the role of miR-181b in extracellular matrix (ECM) degradation. Therefore, we showed that ECM degradation, a critical step in CAVD, might be mediated by the miR-181b/TIMP3 pathway. In Aim 2, we focused on studying the novel shear-sensitive miR-483-3p. We discovered that it regulated inflammation and endothelial-to-mesenchymal transition (EndMT) in HAVECs. In HAVECs we identified UBE2C as a novel shear-sensitive gene targeted by miR-483; which regulates endothelial inflammation and EndMT. Additionally, UBE2C exerts… Advisors/Committee Members: Jo, Hanjoong (advisor), Taylor, W. Robert (committee member), Nerem, Robert M. (committee member), Yoganathan, Ajit P. (committee member), Wilkinson, Keith D. (committee member), Garcia, Andres (committee member).

Subjects/Keywords: OS; miRNA; HAVECs; LS; TIMP3; UBE2C; HIF1A; pVHL; KLF2; Inflammation; Aortic valve; Calcification

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APA (6^th Edition):

Fernandez Esmerats, J. (2018). The role of flow-sensitive MiRNAs and UBE2C-dependent HIF1α pathway in calcific aortic valve disease. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/62206

Chicago Manual of Style (16^th Edition):

Fernandez Esmerats, Joan. “The role of flow-sensitive MiRNAs and UBE2C-dependent HIF1α pathway in calcific aortic valve disease.” 2018. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/62206.

MLA Handbook (7^th Edition):

Fernandez Esmerats, Joan. “The role of flow-sensitive MiRNAs and UBE2C-dependent HIF1α pathway in calcific aortic valve disease.” 2018. Web. 16 Apr 2021.

Vancouver:

Fernandez Esmerats J. The role of flow-sensitive MiRNAs and UBE2C-dependent HIF1α pathway in calcific aortic valve disease. [Internet] [Doctoral dissertation]. Georgia Tech; 2018. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/62206.

Council of Science Editors:

Fernandez Esmerats J. The role of flow-sensitive MiRNAs and UBE2C-dependent HIF1α pathway in calcific aortic valve disease. [Doctoral Dissertation]. Georgia Tech; 2018. Available from: http://hdl.handle.net/1853/62206

Georgia Tech

10. Doroudi, Maryam. Essential roles of Pdia3/PLAA receptor complex and CaMKII IN 1α,25(OH)₂D₃ and Wnt5a calcium-dependent signaling pathways in osteoblasts and chondrocytes.

Degree: PhD, Biology, 2014, Georgia Tech

URL: http://hdl.handle.net/1853/53427

► The vitamin D metabolite 1,25-dihydroxyvitamin D3 [1α,25(OH)2D3] plays an important role in the regulation of musculoskeletal growth and differentiation. 1α,25(OH)2D3 mediates its effects on cells,… (more)

Subjects/Keywords: 1,25-dihydroxyvitamin D3; Growth plate

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APA (6^th Edition):

Doroudi, M. (2014). Essential roles of Pdia3/PLAA receptor complex and CaMKII IN 1α,25(OH)₂D₃ and Wnt5a calcium-dependent signaling pathways in osteoblasts and chondrocytes. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/53427

Chicago Manual of Style (16^th Edition):

Doroudi, Maryam. “Essential roles of Pdia3/PLAA receptor complex and CaMKII IN 1α,25(OH)₂D₃ and Wnt5a calcium-dependent signaling pathways in osteoblasts and chondrocytes.” 2014. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/53427.

MLA Handbook (7^th Edition):

Doroudi, Maryam. “Essential roles of Pdia3/PLAA receptor complex and CaMKII IN 1α,25(OH)₂D₃ and Wnt5a calcium-dependent signaling pathways in osteoblasts and chondrocytes.” 2014. Web. 16 Apr 2021.

Vancouver:

Doroudi M. Essential roles of Pdia3/PLAA receptor complex and CaMKII IN 1α,25(OH)₂D₃ and Wnt5a calcium-dependent signaling pathways in osteoblasts and chondrocytes. [Internet] [Doctoral dissertation]. Georgia Tech; 2014. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/53427.

Council of Science Editors:

Doroudi M. Essential roles of Pdia3/PLAA receptor complex and CaMKII IN 1α,25(OH)₂D₃ and Wnt5a calcium-dependent signaling pathways in osteoblasts and chondrocytes. [Doctoral Dissertation]. Georgia Tech; 2014. Available from: http://hdl.handle.net/1853/53427

Georgia Tech

11. Yap, Choon Hwai. The fluid shear stress environment of the normal and congenital bicuspid aortic valve and the implications on valve calcification.

Degree: PhD, Biomedical Engineering, 2011, Georgia Tech

URL: http://hdl.handle.net/1853/45742

► Calcific aortic valve disease is highly prevalent, especially in the elderly. Currently, the exact mechanism of the calcification process is not completely understood, limiting our… (more)

▼ Calcific aortic valve disease is highly prevalent, especially in the elderly. Currently, the exact mechanism of the calcification process is not completely understood, limiting our ability to prevent or cure the disease. Ex vivo investigations, however, have provided evidence that the aortic valve's biological response is sensitive to mechanical forces, including fluid shear stresses, leading to the hypothesis that adverse fluid shear stress environment play a role in leading to valve calcification. This thesis seeks to investigate this hypothesis. A method for performing experimental measurement of time-varying shear stress on aortic valve leaflets under physiologic flow conditions was first developed, based on the Laser Doppler Velocimetry technique, and was systematically validated. This method was then applied to both the aortic surface and the ventricular surface of a normal tricuspid the aortic valve, and then on a congenital bicuspid aortic valve, using suitable in vitro valve models and an in vitro pulsatile flow loop. It was found that in the tricuspid valve, the peak shear stress on the aortic surface under adult resting condition was approximately 15-19 dyn/cm². Aortic surface shear stresses were elevated during mid- to late-systole, with the development of the sinus vortex, and were low during all other instances. Aortic surface shear stresses were observed to increase with increasing stroke volume and with decreasing heart rate. On the ventricular surface, shear stresses had a systolic peak of approximately 64-71 dyn/cm² under adult resting conditions. During late systole, due to the Womersley effect, shear stresses were observed to reverse in direction to a substantial magnitude for a substantial period of time. Further, it was found that a moderately stenotic bicuspid aortic valve can experience excessive unsteadiness in shear stress experienced by its leaflets, most likely due to the turbulent forward flow resulting from the stenosis, and due to the skewed forward flow. To demonstrate that the measured shear stresses can have an effect on the aortic valve biology, ex vivo experiments were performed in specific to determine the effects of these various shear stress characteristics on the biological response of porcine aortic valve leaflets, using the cone and plate bioreactor. It was found that unsteady shear stress measured in the bicuspid valve resulted in increased calcium accumulation. Further, it was found that low shear stresses and high frequency shear stresses resulted in increased calcium accumulation. Thus, shear stress was found to affect aortic valve pathology, and low and unsteady fluid shear stresses can enhance pathology. Advisors/Committee Members: Yoganathan, Ajit P. (Committee Chair), Giddens, Don P. (Committee Member), Gleason, Rudolph L. Jr. (Committee Member), Glezer, Ari (Committee Member), Jo, Hanjoong (Committee Member), Taylor, W. Robert (Committee Member).

Subjects/Keywords: Bicuspid aortic valve; Laser doppler velocimetry; Cone and plate bioreactor; Shear stress; Fluid mechanics; Aortic valve; Aortic valve calcification disease; Aortic valve Diseases; Aortic valve insufficiency; Aortic valve Stenosis; Mitral valve

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APA (6^th Edition):

Yap, C. H. (2011). The fluid shear stress environment of the normal and congenital bicuspid aortic valve and the implications on valve calcification. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/45742

Chicago Manual of Style (16^th Edition):

Yap, Choon Hwai. “The fluid shear stress environment of the normal and congenital bicuspid aortic valve and the implications on valve calcification.” 2011. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/45742.

MLA Handbook (7^th Edition):

Yap, Choon Hwai. “The fluid shear stress environment of the normal and congenital bicuspid aortic valve and the implications on valve calcification.” 2011. Web. 16 Apr 2021.

Vancouver:

Yap CH. The fluid shear stress environment of the normal and congenital bicuspid aortic valve and the implications on valve calcification. [Internet] [Doctoral dissertation]. Georgia Tech; 2011. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/45742.

Council of Science Editors:

Yap CH. The fluid shear stress environment of the normal and congenital bicuspid aortic valve and the implications on valve calcification. [Doctoral Dissertation]. Georgia Tech; 2011. Available from: http://hdl.handle.net/1853/45742

12. Yin, Weiwei. The role and regulatory mechanisms of nox1 in vascular systems.

Degree: PhD, Biomedical Engineering, 2012, Georgia Tech

URL: http://hdl.handle.net/1853/44833

► As an important endogenous source of reactive oxygen species (ROS), NADPH oxidase 1 (Nox1) has received tremendous attention in the past few decades. It has… (more)

▼ As an important endogenous source of reactive oxygen species (ROS), NADPH oxidase 1 (Nox1) has received tremendous attention in the past few decades. It has been identified to play a key role as the initial "kindle," whose activation is crucial for amplifying ROS production through several propagation mechanisms in the vascular system. As a consequence, Nox1 has been implicated in the initiation and genesis of many cardiovascular diseases and has therefore been the subject of detailed investigations. The literature on experimental studies of the Nox1 system is extensive. Numerous investigations have identified essential features of the Nox1 system in vasculature and characterized key components, possible regulatory signals and/or signaling pathways, potential activation mechanisms, a variety of Nox1 stimuli, and its potential physiological and pathophysiological functions. While these experimental studies have greatly enhanced our understanding of the Nox1 system, many open questions remain regarding the overall functionality and dynamic behavior of Nox1 in response to specific stimuli. Such questions include the following. What are the main regulatory and/or activation mechanisms of Nox1 systems in different types of vascular cells? Once Nox1 is activated, how does the system return to its original, unstimulated state, and how will its subunits be recycled? What are the potential disassembly pathways of Nox1? Are these pathways equally important for effectively reutilizing Nox1 subunits? How does Nox1 activity change in response to dynamic signals? Are there generic features or principles within the Nox1 system that permit optimal performance? These types of questions have not been answered by experiments, and they are indeed quite difficult to address with experiments. I demonstrate in this dissertation that one can pose such questions and at least partially answer them with mathematical and computational methods. Two specific cell types, namely endothelial cells (ECs) and vascular smooth muscle cells (VSMCs), are used as "templates" to investigate distinct modes of regulation of Nox1 in different vascular cells. By using a diverse array of modeling methods and computer simulations, this research identifies different types of regulation and their distinct roles in the activation process of Nox1. In the first study, I analyze ECs stimulated by mechanical stimuli, namely shear stresses of different types. The second study uses different analytical and simulation methods to reveal generic features of alternative disassembly mechanisms of Nox1 in VSMCs. This study leads to predictions of the overall dynamic behavior of the Nox1 system in VSMCs as it responds to extracellular stimuli, such as the hormone angiotensin II. The studies and investigations presented here improve our current understanding of the Nox1 system in the vascular system and might help us to develop potential strategies for manipulation and controlling Nox1 activity, which in turn will benefit future experimental and clinical studies. Advisors/Committee Members: Kemp, Melissa (Committee Chair), Griendling, Kathy (Committee Member), Jo, Hanjoong (Committee Member), Platt, Manu (Committee Member), Voit, Eberhard (Committee Member).

Subjects/Keywords: Atherosclerosis; Mechanotransduction; NADPH oxidase 1; Computational model; Biochemical systems theory; System biology; Cardiovascular system; Design princple; Reactive oxygen species; Pathway analysis; Multi-scale system modeling; Signaling pathway modeling; Monte Carlo method; Dynamic simulation; Endothelium; Nitric oxide; Active oxygen

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APA (6^th Edition):

Yin, W. (2012). The role and regulatory mechanisms of nox1 in vascular systems. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/44833

Chicago Manual of Style (16^th Edition):

Yin, Weiwei. “The role and regulatory mechanisms of nox1 in vascular systems.” 2012. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/44833.

MLA Handbook (7^th Edition):

Yin, Weiwei. “The role and regulatory mechanisms of nox1 in vascular systems.” 2012. Web. 16 Apr 2021.

Vancouver:

Yin W. The role and regulatory mechanisms of nox1 in vascular systems. [Internet] [Doctoral dissertation]. Georgia Tech; 2012. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/44833.

Council of Science Editors:

Yin W. The role and regulatory mechanisms of nox1 in vascular systems. [Doctoral Dissertation]. Georgia Tech; 2012. Available from: http://hdl.handle.net/1853/44833

13. Zhong, Ming. Apoptotic signaling pathways in mammalian growth plate chondrocytes.

Degree: PhD, Biomedical Engineering, 2010, Georgia Tech

URL: http://hdl.handle.net/1853/33993

► The growth plate resting zone consists of hyaline-like chondrocytes disbursed in a proteoglycan rich extracellular matrix. These cells give rise to the columns of the… (more)

▼ The growth plate resting zone consists of hyaline-like chondrocytes disbursed in a proteoglycan rich extracellular matrix. These cells give rise to the columns of the growth zone, consisting of progressively hypertrophic cells. Proliferation of resting zone chondrocytes induced by systemic and local stimuli is the driving force of longitudinal growth of long bones. Therefore, homeostasis of this cell population has great importance. Although the regulation of proliferation and differentiation of these cells has been well studied, little is known about the regulation of their apoptosis. We have previously shown that chelerythrine and tamoxifen induce apoptosis in resting zone chondrocytes in a nitric oxide (NO)-dependent pathway. In this study we explored two physiological apoptogens: inorganic phosphate (Pi) and 17β-estradiol (E₂). We found NO production is necessary in Pi-induced apoptosis. We also found that NO donors induced chondrocyte apoptosis by up-regulating p53 expression, Bax/Bcl-2 expression ratio and cytochrome C release from mitochondria, as well as caspase-3 activity, indicating that NO induces chondrocyte apoptosis in a mitochondrial pathway. Mitogen activated protein kinase (MAPK) activity was involved. A c-Jun N-terminal kinase (JNK) inhibitor, but not inhibitors of p38 or extracellular signal-regulated kinase (ERK1/2), was able to block NO-induced apoptosis, indicating that JNK is necessary in this pathway. Taken together, Pi elevates NO production, which leads to a mitochondrial apoptotic pathway dependent on JNK. On the other hand, although E₂caused apoptosis in resting zone chondrocytes in a dose-dependent manner, up-regulated p53 and Bax, and induced release of cytochrome C from the mitochondria, which indicated a mitochondrial apoptotic pathway, the apoptosis did not involve elevated nitric oxide production or MAPK as was found in Pi-induced apoptosis. This study elucidates the signaling pathway underlying Pi and E₂-induced chondrocyte apoptosis. It has important implications on understanding the development of mammalian growth plate. It also provides further information about the physiological functions of estrogen on longitudinal bone growth. Advisors/Committee Members: Boyan, Barbara (Committee Chair), Carney, Darrell (Committee Member), Jo, Hanjoong (Committee Member), Lobachev, Kirill (Committee Member), Schwartz, Zvi (Committee Member).

Subjects/Keywords: Apoptosis; MAP kinases; Nitric oxide; Phosphates; P53; Estrogen; Growth plate chondrocytes; Endochondral ossification; Growth plate; Bones Growth; Cartilage; Bone; Ossification

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APA (6^th Edition):

Zhong, M. (2010). Apoptotic signaling pathways in mammalian growth plate chondrocytes. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/33993

Chicago Manual of Style (16^th Edition):

Zhong, Ming. “Apoptotic signaling pathways in mammalian growth plate chondrocytes.” 2010. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/33993.

MLA Handbook (7^th Edition):

Zhong, Ming. “Apoptotic signaling pathways in mammalian growth plate chondrocytes.” 2010. Web. 16 Apr 2021.

Vancouver:

Zhong M. Apoptotic signaling pathways in mammalian growth plate chondrocytes. [Internet] [Doctoral dissertation]. Georgia Tech; 2010. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/33993.

Council of Science Editors:

Zhong M. Apoptotic signaling pathways in mammalian growth plate chondrocytes. [Doctoral Dissertation]. Georgia Tech; 2010. Available from: http://hdl.handle.net/1853/33993

14. Sargent, Carolyn Yeago. Effects of hydrodynamic culture on embryonic stem cell differentiation: cardiogenic modulation.

Degree: PhD, Biomedical Engineering, 2010, Georgia Tech

URL: http://hdl.handle.net/1853/34710

► Stem and progenitor cells are an attractive cell source for the treatment of degenerative diseases due to their potential to differentiate into multiple cell types… (more)

Subjects/Keywords: Embryonic stem cells; Embryoid body; Hydrodynamic; Bioprocessing; Differentiation; Cardiomyocyte; Heart cells; Degeneration (Pathology); Hydrodynamics; Embryonic stem cells Research

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APA (6^th Edition):

Sargent, C. Y. (2010). Effects of hydrodynamic culture on embryonic stem cell differentiation: cardiogenic modulation. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/34710

Chicago Manual of Style (16^th Edition):

Sargent, Carolyn Yeago. “Effects of hydrodynamic culture on embryonic stem cell differentiation: cardiogenic modulation.” 2010. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/34710.

MLA Handbook (7^th Edition):

Sargent, Carolyn Yeago. “Effects of hydrodynamic culture on embryonic stem cell differentiation: cardiogenic modulation.” 2010. Web. 16 Apr 2021.

Vancouver:

Sargent CY. Effects of hydrodynamic culture on embryonic stem cell differentiation: cardiogenic modulation. [Internet] [Doctoral dissertation]. Georgia Tech; 2010. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/34710.

Council of Science Editors:

Sargent CY. Effects of hydrodynamic culture on embryonic stem cell differentiation: cardiogenic modulation. [Doctoral Dissertation]. Georgia Tech; 2010. Available from: http://hdl.handle.net/1853/34710

15. Simmons, Rachel Diane. MIR-744 modulation by disturbed flow and its role in endothelial inflammation and atherosclerosis.

Degree: PhD, Biomedical Engineering (Joint GT/Emory Department), 2017, Georgia Tech

URL: http://hdl.handle.net/1853/60679

► Atherosclerosis is the leading cause of death in developed nations as it is the underlying cause of many cardiovascular diseases (CVD) such as myocardial infarction,… (more)

Subjects/Keywords: miRNAs; Hemodynamics; Atherosclerosis; Endothelial inflammation

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APA (6^th Edition):

Simmons, R. D. (2017). MIR-744 modulation by disturbed flow and its role in endothelial inflammation and atherosclerosis. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/60679

Chicago Manual of Style (16^th Edition):

Simmons, Rachel Diane. “MIR-744 modulation by disturbed flow and its role in endothelial inflammation and atherosclerosis.” 2017. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/60679.

MLA Handbook (7^th Edition):

Simmons, Rachel Diane. “MIR-744 modulation by disturbed flow and its role in endothelial inflammation and atherosclerosis.” 2017. Web. 16 Apr 2021.

Vancouver:

Simmons RD. MIR-744 modulation by disturbed flow and its role in endothelial inflammation and atherosclerosis. [Internet] [Doctoral dissertation]. Georgia Tech; 2017. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/60679.

Council of Science Editors:

Simmons RD. MIR-744 modulation by disturbed flow and its role in endothelial inflammation and atherosclerosis. [Doctoral Dissertation]. Georgia Tech; 2017. Available from: http://hdl.handle.net/1853/60679

16. Holliday, Casey Jane. Discovery of shear- and side-dependent messenger RNAs and microRNAs in aortic valvular endothelium.

Degree: PhD, Biomedical Engineering, 2012, Georgia Tech

URL: http://hdl.handle.net/1853/47517

► Aortic valve (AV) disease is a major cause of cardiovascular-linked deaths globally. In addition, AV disease is a strong risk factor for additional cardiovascular events;… (more)

▼ Aortic valve (AV) disease is a major cause of cardiovascular-linked deaths globally. In addition, AV disease is a strong risk factor for additional cardiovascular events; however, the mechanism by which it initiates and progresses is not well-understood. We hypothesize that low and oscillatory flow is present on the fibrosa side of the AV and stimulates ECs to differentially regulate microRNA (miRNA) and mRNAs and influence AV disease progression. This hypothesis was tested employing both in vitro and in vivo approaches, high throughput microarray and pathway analyses, as well as a variety of functional assays. First, we isolated and characterized side-dependent, human aortic valvular endothelial cells (HAVECs). We found that HAVECs express both endothelial cell markers (VE-Cadherin, vWF, and PECAM) as well as smooth muscle cell markers (SMA and basic calponin). Using microarray analysis on sheared, side-specific HAVECs, we identified side- and shear-induced changes in miRNA and mRNA expression profiles. More specifically, we identified over 1000 shear-responsive mRNAs which showed robust validation (93% of those tested). We then used Ingenuity Pathway Analysis to identify key miRNAs, including those with many relationships to other genes (for example, thrombospondin and I&B) and those that are members of over-represented pathways and processes (for example, sulfur metabolism). Furthermore, we validated five shear-sensitive miRNAs: miR-139-3p, miR-148a, miR-187, miR-192, and miR-486-5p and one side-dependent miRNA, miR-370. To prioritize these miRNAs, we performed in silico analysis to group these key miRNAs by cellular functions related to AV disease (including tissue remodeling, inflammation, and calcification). Next, to compare our in vitro HAVEC results in vivo, we developed a method to isolate endothelial-enriched, side-dependent total RNA and identify and validate side-dependent (fibrosa vs. ventricularis) miRNAs in porcine aortic valvular endothelium. From this analysis, we discovered and validated eight side-dependent miRNAs in porcine endothelial-enriched AV RNA, including one miRNA previously identified in vitro, miR-486-5p. Lastly, we determined the relationship between important miRNAs (specifically miR-187 and miR-486-5p) and AV disease by modulating levels of miRNAs and performing functional assays. Preliminary studies overexpressing miR-187 in HAVECs have shown a reduction in inflammatory state through monocyte adhesion (p<0.05). Further, miR-486-5p overexpression reveals an increase in migration (p<0.05) and a trend for a decrease in early apoptosis, linking miR-486-5p to tissue remodeling in the AV. Better understanding of AV biology and disease in terms of gene-regulation under different hemodynamic conditions will facilitate the design of a tissue-engineered valve and provide alternative treatment options. Advisors/Committee Members: Jo, Hanjoong (Committee Co-Chair), Nerem, Robert. M (Committee Co-Chair), Eskin, Suzanne (Committee Member), Taylor, W. Robert (Committee Member), Thourani, Vinod (Committee Member), Yoganathan, Ajit (Committee Member).

Subjects/Keywords: Aortic valve; Endothelium; MicroRNAs; Shear stress; Microarrays; MRNAs; Aortic valve Diseases; Aortic valve Stenosis; Messenger RNA; Vascular endothelium

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APA (6^th Edition):

Holliday, C. J. (2012). Discovery of shear- and side-dependent messenger RNAs and microRNAs in aortic valvular endothelium. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/47517

Chicago Manual of Style (16^th Edition):

Holliday, Casey Jane. “Discovery of shear- and side-dependent messenger RNAs and microRNAs in aortic valvular endothelium.” 2012. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/47517.

MLA Handbook (7^th Edition):

Holliday, Casey Jane. “Discovery of shear- and side-dependent messenger RNAs and microRNAs in aortic valvular endothelium.” 2012. Web. 16 Apr 2021.

Vancouver:

Holliday CJ. Discovery of shear- and side-dependent messenger RNAs and microRNAs in aortic valvular endothelium. [Internet] [Doctoral dissertation]. Georgia Tech; 2012. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/47517.

Council of Science Editors:

Holliday CJ. Discovery of shear- and side-dependent messenger RNAs and microRNAs in aortic valvular endothelium. [Doctoral Dissertation]. Georgia Tech; 2012. Available from: http://hdl.handle.net/1853/47517

17. Boopathy, Archana Vidya. Engineering stem cell responses using oxidative stress and notch ligand containing hydrogels.

Degree: PhD, Biomedical Engineering (Joint GT/Emory Department), 2014, Georgia Tech

URL: http://hdl.handle.net/1853/51837

► Heart failure is the leading cause of death worldwide. In 2013, the American Heart Association estimated that one American will die of cardiovascular disease every… (more)

Subjects/Keywords: Adult stem cells; Notch; Hydrogel; Oxidative stress; Myocardial infarction; Colloids in medicine; Biocolloids; Myocardium Regeneration; Mesenchymal stem cells; Oxidative stress; Notch genes

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APA (6^th Edition):

Boopathy, A. V. (2014). Engineering stem cell responses using oxidative stress and notch ligand containing hydrogels. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/51837

Chicago Manual of Style (16^th Edition):

Boopathy, Archana Vidya. “Engineering stem cell responses using oxidative stress and notch ligand containing hydrogels.” 2014. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/51837.

MLA Handbook (7^th Edition):

Boopathy, Archana Vidya. “Engineering stem cell responses using oxidative stress and notch ligand containing hydrogels.” 2014. Web. 16 Apr 2021.

Vancouver:

Boopathy AV. Engineering stem cell responses using oxidative stress and notch ligand containing hydrogels. [Internet] [Doctoral dissertation]. Georgia Tech; 2014. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/51837.

Council of Science Editors:

Boopathy AV. Engineering stem cell responses using oxidative stress and notch ligand containing hydrogels. [Doctoral Dissertation]. Georgia Tech; 2014. Available from: http://hdl.handle.net/1853/51837

18. Dunn, Jessilyn. Genome-scale DNA methylation changes in endothelial cells by disturbed flow and its role in atherosclerosis.

Degree: PhD, Biomedical Engineering (Joint GT/Emory Department), 2015, Georgia Tech

URL: http://hdl.handle.net/1853/53536

► Atherosclerosis is an inflammatory disease of the arterial walls and is the major cause of heart attack and stroke. Atherosclerosis is localized to curves or… (more)

Subjects/Keywords: DNMT; Transcriptome; Shear stress; Disturbed flow; Atherosclerosis; HoxA5; Klf3; Endothelial cells; DNA methylome; Gene expression

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APA (6^th Edition):

Dunn, J. (2015). Genome-scale DNA methylation changes in endothelial cells by disturbed flow and its role in atherosclerosis. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/53536

Chicago Manual of Style (16^th Edition):

Dunn, Jessilyn. “Genome-scale DNA methylation changes in endothelial cells by disturbed flow and its role in atherosclerosis.” 2015. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/53536.

MLA Handbook (7^th Edition):

Dunn, Jessilyn. “Genome-scale DNA methylation changes in endothelial cells by disturbed flow and its role in atherosclerosis.” 2015. Web. 16 Apr 2021.

Vancouver:

Dunn J. Genome-scale DNA methylation changes in endothelial cells by disturbed flow and its role in atherosclerosis. [Internet] [Doctoral dissertation]. Georgia Tech; 2015. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/53536.

Council of Science Editors:

Dunn J. Genome-scale DNA methylation changes in endothelial cells by disturbed flow and its role in atherosclerosis. [Doctoral Dissertation]. Georgia Tech; 2015. Available from: http://hdl.handle.net/1853/53536

19. Prasanphanich, Adam Franklin. Dynamic redox signaling during TGF-beta-induced epithelial-mesenchymal transition.

Degree: PhD, Biomedical Engineering (Joint GT/Emory Department), 2015, Georgia Tech

URL: http://hdl.handle.net/1853/56163

► Individual biological processes operate within larger contexts and can participate in the emergence of complex phenotypes. The morphogen transforming growth factor β (TGFβ) can initiate… (more)

▼ Individual biological processes operate within larger contexts and can participate in the emergence of complex phenotypes. The morphogen transforming growth factor β (TGFβ) can initiate diverse cellular responses, including down-regulation of numerous antioxidant species. TGFβ signaling itself has been shown to exhibit redox sensitivity and in the context of TGFβ-mediated epithelial-mesenchymal transition (EMT), there exists a possibility of a positive feedback loop operating over multiple temporal and biological scales to stabilize a mesenchymal phenotype. Additionally, drug resistant side populations (SP) arise in populations that exhibit heterogeneity of ABCG2 transporter activity, which is regulated within the same cellular program as antioxidants. Therefore, it is possible that SPs reflect heterogeneity in redox regulation within a population; however, how single-cell ABCG2 activity heterogeneity manifests at the population level is not known. The overall objective of this research was to investigate how redox regulated processes contribute to complex phenotypes that arise in the context of TGFβ-mediated EMT using multivariate and systems approaches. We investigated the dynamics of redox regulation in the context of EMT, hypothesizing that decreased nucleophilic tone acquired during EMT strengthens TGFβ signaling enhancing acquisition and stabilization of the mesenchymal phenotype. We demonstrated the sensitivity of TGFβ signaling to antioxidants and the down-regulation of antioxidants within a singular model. We developed in-cell western assays to evaluate multivariate phenotype states as they developed during EMT. TGFβ treatment decreased H2O2 degradation rates and increased glutathione redox potential, indicating decreased nucleophilic tone. Epithelial/mesenchymal differentiation and redox time course data were paired using principal component analysis (PCA) to construct a multivariate representation of phenotype over the time course of EMT. We found that decreased nucleophilic tone during EMT coincides with acquisition of a mesenchymal phenotype over too long a time scale to enable enhancement of EMT. In the second portion of this research, we investigated the role of heterogeneity of ABCG2 activity at the single cell level in the emergence of SPs at the population level and the means by which TGFβ signaling modulates heterogeneity to affect SP size. TGFβ was found to decrease the size of SPs as well as the magnitude of response. A multiscale ensemble model consisting of a heterogeneous population of individual cells was used to interrogate multiple kinetic schemas and identified a highly active subpopulation juxtaposed by an inactive main population, suggesting the SP cells may exhibit a distinct redox profile from main cells, the frequency of which was decreased in response to TGFβ. In summary, we developed an approach to investigate the dynamics of redox regulation during TGFβ-mediated EMT from the perspective of a multivariate phenotype, simultaneously accounting for changes in epithelial/mesenchymal… Advisors/Committee Members: Kemp, Melissa L (advisor), Barker, Thomas H. (committee member), Jo, Hanjoong (committee member), Medford, Russell M. (committee member), Voit, Eberhard O. (committee member).

Subjects/Keywords: TGF-beta; Computational modeling; Redox biology

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APA (6^th Edition):

Prasanphanich, A. F. (2015). Dynamic redox signaling during TGF-beta-induced epithelial-mesenchymal transition. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/56163

Chicago Manual of Style (16^th Edition):

Prasanphanich, Adam Franklin. “Dynamic redox signaling during TGF-beta-induced epithelial-mesenchymal transition.” 2015. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/56163.

MLA Handbook (7^th Edition):

Prasanphanich, Adam Franklin. “Dynamic redox signaling during TGF-beta-induced epithelial-mesenchymal transition.” 2015. Web. 16 Apr 2021.

Vancouver:

Prasanphanich AF. Dynamic redox signaling during TGF-beta-induced epithelial-mesenchymal transition. [Internet] [Doctoral dissertation]. Georgia Tech; 2015. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/56163.

Council of Science Editors:

Prasanphanich AF. Dynamic redox signaling during TGF-beta-induced epithelial-mesenchymal transition. [Doctoral Dissertation]. Georgia Tech; 2015. Available from: http://hdl.handle.net/1853/56163

20. Caulk, Alexander Wilson. Biomechanics and modeling methods for quantifying mechanically-mediated disease progression in neglected populations.

Degree: PhD, Mechanical Engineering, 2015, Georgia Tech

URL: http://hdl.handle.net/1853/55490

► It is well known that biological tissue grows and remodels in response to changes in mechanical loading. Arteries and lymphatic vessels share many similar mechanical… (more)

Subjects/Keywords: Biomechanics; HIV; HAART; lymphedema; growth and remodeling; constitutive modeling

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APA (6^th Edition):

Caulk, A. W. (2015). Biomechanics and modeling methods for quantifying mechanically-mediated disease progression in neglected populations. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/55490

Chicago Manual of Style (16^th Edition):

Caulk, Alexander Wilson. “Biomechanics and modeling methods for quantifying mechanically-mediated disease progression in neglected populations.” 2015. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/55490.

MLA Handbook (7^th Edition):

Caulk, Alexander Wilson. “Biomechanics and modeling methods for quantifying mechanically-mediated disease progression in neglected populations.” 2015. Web. 16 Apr 2021.

Vancouver:

Caulk AW. Biomechanics and modeling methods for quantifying mechanically-mediated disease progression in neglected populations. [Internet] [Doctoral dissertation]. Georgia Tech; 2015. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/55490.

Council of Science Editors:

Caulk AW. Biomechanics and modeling methods for quantifying mechanically-mediated disease progression in neglected populations. [Doctoral Dissertation]. Georgia Tech; 2015. Available from: http://hdl.handle.net/1853/55490

21. Sy, Jay Christopher. Novel strategies for cardiac drug delivery.

Degree: PhD, Biomedical Engineering, 2011, Georgia Tech

URL: http://hdl.handle.net/1853/39531

► The American Heart Association (AHA) estimates that at least one American will die from a coronary event every minute, costing over $150 billion in 2008… (more)

Subjects/Keywords: Cardiac dysfunction; Myocardial infarction; Necrosis; Hoechst; Nitrilotriacetic acid; Polyketals; Biomaterials; Heart disease; Drug delivery; Drug delivery systems; Guided tissue regeneration

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APA (6^th Edition):

Sy, J. C. (2011). Novel strategies for cardiac drug delivery. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/39531

Chicago Manual of Style (16^th Edition):

Sy, Jay Christopher. “Novel strategies for cardiac drug delivery.” 2011. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/39531.

MLA Handbook (7^th Edition):

Sy, Jay Christopher. “Novel strategies for cardiac drug delivery.” 2011. Web. 16 Apr 2021.

Vancouver:

Sy JC. Novel strategies for cardiac drug delivery. [Internet] [Doctoral dissertation]. Georgia Tech; 2011. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/39531.

Council of Science Editors:

Sy JC. Novel strategies for cardiac drug delivery. [Doctoral Dissertation]. Georgia Tech; 2011. Available from: http://hdl.handle.net/1853/39531

Georgia Tech

22. Bellott, Anne Claire. The Role of Caveolae in the Loss of ERK2 Activation in Stretched Skeletal Myotubes.

Degree: MS, Mechanical Engineering, 2004, Georgia Tech

URL: http://hdl.handle.net/1853/5075

► Skeletal muscle function is important to the human body for daily activities. Mechanical signals are critical to the maintenance of that function. Muscle diseases, such… (more)

Subjects/Keywords: Skeletal muscle; ERK2; Mechanotransduction; Caveolae; Caveolin-3

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APA (6^th Edition):

Bellott, A. C. (2004). The Role of Caveolae in the Loss of ERK2 Activation in Stretched Skeletal Myotubes. (Masters Thesis). Georgia Tech. Retrieved from http://hdl.handle.net/1853/5075

Chicago Manual of Style (16^th Edition):

Bellott, Anne Claire. “The Role of Caveolae in the Loss of ERK2 Activation in Stretched Skeletal Myotubes.” 2004. Masters Thesis, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/5075.

MLA Handbook (7^th Edition):

Bellott, Anne Claire. “The Role of Caveolae in the Loss of ERK2 Activation in Stretched Skeletal Myotubes.” 2004. Web. 16 Apr 2021.

Vancouver:

Bellott AC. The Role of Caveolae in the Loss of ERK2 Activation in Stretched Skeletal Myotubes. [Internet] [Masters thesis]. Georgia Tech; 2004. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/5075.

Council of Science Editors:

Bellott AC. The Role of Caveolae in the Loss of ERK2 Activation in Stretched Skeletal Myotubes. [Masters Thesis]. Georgia Tech; 2004. Available from: http://hdl.handle.net/1853/5075

Georgia Tech

23. Wong, Kevin L. Caveolae and Caveolin-1 are important for Vitamin D signalling.

Degree: MS, Biomedical Engineering, 2010, Georgia Tech

URL: http://hdl.handle.net/1853/37086

► The most active form of Vitamin D, 1alpha,25(OH)2D3, modulates cells via receptor mediated mechanisms. While studies have elucidated the pathway via the classical nuclear Vitamin… (more)

Subjects/Keywords: Chondrocytes; Lipid raft; Cav-1 knockout mice; Matrix vesicles; Protein kinase C; Cartilage cells; Human physiology; Cholecalciferol; Vitamin D

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

APA (6^th Edition):

Wong, K. L. (2010). Caveolae and Caveolin-1 are important for Vitamin D signalling. (Masters Thesis). Georgia Tech. Retrieved from http://hdl.handle.net/1853/37086

Chicago Manual of Style (16^th Edition):

Wong, Kevin L. “Caveolae and Caveolin-1 are important for Vitamin D signalling.” 2010. Masters Thesis, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/37086.

MLA Handbook (7^th Edition):

Wong, Kevin L. “Caveolae and Caveolin-1 are important for Vitamin D signalling.” 2010. Web. 16 Apr 2021.

Vancouver:

Wong KL. Caveolae and Caveolin-1 are important for Vitamin D signalling. [Internet] [Masters thesis]. Georgia Tech; 2010. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/37086.

Council of Science Editors:

Wong KL. Caveolae and Caveolin-1 are important for Vitamin D signalling. [Masters Thesis]. Georgia Tech; 2010. Available from: http://hdl.handle.net/1853/37086

Georgia Tech

24. Tressel, Sarah Lynne. Role of shear stress in angiopoietin-2-dependent neovascularization: implications in occlusive vascular disease and atherosclerosis.

Degree: PhD, Biomedical Engineering, 2008, Georgia Tech

URL: http://hdl.handle.net/1853/22646

► Neovascularization, or the formation of blood vessels, is important in both normal physiological processes as well as pathophysiological processes. The main players in neovascularization, endothelial… (more)

▼ Neovascularization, or the formation of blood vessels, is important in both normal physiological processes as well as pathophysiological processes. The main players in neovascularization, endothelial cells (EC), are highly influenced by hemodynamic shear stress and this may play an important role in neovascularization. Two typical types of shear stress found in the vascular system are a unidirectional laminar shear stress (LS) found in straight regions and a disturbed, oscillatory shear stress (OS) found at branches or curves. At the cellular level, LS is thought to promote EC quiescence whereas OS is thought to promote EC dysfunction. Oscillatory sheared EC are pro-proliferative, pro-migratory, and secrete growth factors, all functions important in neovascularization. There are several diseases that involve both disturbed shear stress and neovascularization, such as atherosclerosis, aortic valve disease, and occlusive vascular disease. In these pathophysiological scenarios fluid shear stress may provide a driving force for neovascularization. Therefore, we hypothesized that oscillatory shear stress promotes greater neovascularization compared to unidirectional laminar shear stress through the secretion of angiogenic factors, which play a physiological role in neovascularization in vivo. To test this hypothesis, we first performed tubule formation and migration assays, two important functions in neovessel formation. We found that OS promotes greater tubule formation and migration of EC as compared to LS and this was mediated through secreted factors. Using gene and protein array analysis, we identified Angiopoietin-2 (Ang2) as being upregulated by OS compared to LS in EC. We found that inhibiting Ang2 blocked OS-mediated tubule formation and migration and that LS-inhibited tubule formation could be rescued by addition of Ang2. In addition, Ang2 was found to be upregulated at sites of disturbed flow in vivo, implicating a physiological role for Ang2. To further investigate the physiological role of Ang2 in neovascularization, we examined the effects of inhibiting Ang2 in a mouse model of hindlimb ischemia, which involves both disturbed flow and neovascularization. We found that Ang2 was upregulated in the ischemic adductor muscle suggesting that it plays a role in recovery during hindlimb ischemia. In addition, we found that inhibiting Ang2 decreased blood flow recovery. Ang2 inhibition resulted in decreased smooth muscle cell coverage of vessels as well as decreased macrophage infiltration. These findings suggest that Ang2 promotes blood flow recovery through the recruitment of smooth muscle cells and formation of collaterals, as well as the recruitment of macrophages that secrete important growth factors and help degrade the extracellular matrix in order for neovascularization to occur. In conclusion, this work illustrates the shear stress regulation of neovessel formation through the expression of Ang2, and the role of Ang2 in neovascularization in vivo. By understanding how angiogenic factors… Advisors/Committee Members: Jo, Hanjoong (Committee Chair), McIntire, Larry (Committee Member), Nie, Shuming (Committee Member), Taylor, Robert (Committee Member), Weyand, Cornelia (Committee Member).

Subjects/Keywords: Hindlimb ischemia; Endothelial cells; Arteriogenesis; Shear stress; Angiopoietin-2; Angiogenesis; Vascular endothelium; Blood-vessels Growth; Shear flow; Neovascularization

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APA (6^th Edition):

Tressel, S. L. (2008). Role of shear stress in angiopoietin-2-dependent neovascularization: implications in occlusive vascular disease and atherosclerosis. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/22646

Chicago Manual of Style (16^th Edition):

Tressel, Sarah Lynne. “Role of shear stress in angiopoietin-2-dependent neovascularization: implications in occlusive vascular disease and atherosclerosis.” 2008. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/22646.

MLA Handbook (7^th Edition):

Tressel, Sarah Lynne. “Role of shear stress in angiopoietin-2-dependent neovascularization: implications in occlusive vascular disease and atherosclerosis.” 2008. Web. 16 Apr 2021.

Vancouver:

Tressel SL. Role of shear stress in angiopoietin-2-dependent neovascularization: implications in occlusive vascular disease and atherosclerosis. [Internet] [Doctoral dissertation]. Georgia Tech; 2008. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/22646.

Council of Science Editors:

Tressel SL. Role of shear stress in angiopoietin-2-dependent neovascularization: implications in occlusive vascular disease and atherosclerosis. [Doctoral Dissertation]. Georgia Tech; 2008. Available from: http://hdl.handle.net/1853/22646

Georgia Tech

25. Xing, Yun. Effects of Mechanical Forces on the Biological Properties of Porcine Aortic Valve Leaflets.

Degree: PhD, Bioengineering, 2005, Georgia Tech

URL: http://hdl.handle.net/1853/6828

► Cardiac valves are dynamic, sophisticated structures which interact closely with the surrounding hemodynamic environment. Altered mechanical stresses, including pressure, shear and bending stresses, are believed… (more)

▼ Cardiac valves are dynamic, sophisticated structures which interact closely with the surrounding hemodynamic environment. Altered mechanical stresses, including pressure, shear and bending stresses, are believed to cause changes in valve biology, but the cellular and molecular events involved in these processes are not well characterized. Therefore, the overall goal of this project is to determine the effects of pressure and shear stress on porcine aortic valve leaflets biology. Results from the pressure study showed that elevated constant pressure (140 and 170 mmHg) causes significant increases in collagen synthesis. The increases were 37.5% and 90% for 140 and 170 mmHg, respectively. No significant differences in DNA and sGAG synthesis were observed under constant pressure. In the cyclic pressure study, the effects of both pressure magnitude and pulse frequency were studied. With the frequency fixed at 1.167 Hz, collagen and sGAG synthesis increased proportionally with mean pressure level. At a fixed pressure level (80-120 mmHg), collagen and sGAG synthesis were slightly increased by 25% and 14% at 0.5 Hz, respectively. DNA synthesis was significantly increased by 72% at 2 Hz. An experiment combining high magnitude (150-190 mmHg) and high frequency (2 Hz) demonstrated significant increases in collagen and sGAG synthesis (collagen: 74%, sGAG: 56%), but no significant changes in cell proliferation. Shear levels ranging from 1 to 80 dyne/cm2 were studied. Scanning electron microscopy results indicated that 48 hrs exposure to shear stress did not alter the circumferential alignment of endothelial cells. Collagen synthesis was significantly enhanced at 9 and 25 dyne/cm2, but not different from static controls under other shear conditions. Leaflets denuded of the endothelium were exposed to identical shear stress and showed very different responses. Collagen synthesis was not affected at any shear levels, but sGAG content was increased at shear of 9, 25 and 40 dyne/cm2. Further studies showed that the increases in collagen synthesis under pressure or shear stress was concurrent with a decline in the expression and activities of cathepsins L and S. This converse relationship between collagen synthesis and cathepsin activity indicated that cathepsins might be involved in valvular ECM remodeling. Advisors/Committee Members: Yoganathan, Ajit (Committee Chair), Hilbert, Steve (Committee Member), Jo, Hanjoong (Committee Member), Nerem, Robert (Committee Member), Wick, Timothy (Committee Member).

Subjects/Keywords: Heart valves; Mechanical forces; Tissue engineering; Shear flow; Strains and stresses; Heart valves; Hemodynamics

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

APA (6^th Edition):

Xing, Y. (2005). Effects of Mechanical Forces on the Biological Properties of Porcine Aortic Valve Leaflets. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/6828

Chicago Manual of Style (16^th Edition):

Xing, Yun. “Effects of Mechanical Forces on the Biological Properties of Porcine Aortic Valve Leaflets.” 2005. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/6828.

MLA Handbook (7^th Edition):

Xing, Yun. “Effects of Mechanical Forces on the Biological Properties of Porcine Aortic Valve Leaflets.” 2005. Web. 16 Apr 2021.

Vancouver:

Xing Y. Effects of Mechanical Forces on the Biological Properties of Porcine Aortic Valve Leaflets. [Internet] [Doctoral dissertation]. Georgia Tech; 2005. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/6828.

Council of Science Editors:

Xing Y. Effects of Mechanical Forces on the Biological Properties of Porcine Aortic Valve Leaflets. [Doctoral Dissertation]. Georgia Tech; 2005. Available from: http://hdl.handle.net/1853/6828

Georgia Tech

26. Sykes, Michelle Christine. Regulation of endothelial gene transcription by shear stress in a manner dependent on p47phox-based NADPH oxidases.

Degree: PhD, Biomedical Engineering, 2008, Georgia Tech

URL: http://hdl.handle.net/1853/24824

► Atherosclerosis occurs preferentially at branches and curves in arteries exposed to disturbed flow while sparing straight portions of arteries exposed to undisturbed flow. In vivo… (more)

▼ Atherosclerosis occurs preferentially at branches and curves in arteries exposed to disturbed flow while sparing straight portions of arteries exposed to undisturbed flow. In vivo and in vitro studies have implicated NADPH oxidases in atherosclerosis and hypertension. Shear stress can induce reactive oxygen species production in endothelial cells from a variety of sources, including NADPH oxidases. Here, we examined the hypothesis that unidirectional laminar shear (LS) and oscillatory shear (OS) would differentially regulate gene expression profiles in NADPH oxidase-dependent and -independent manners, and that these genes would provide novel molecular targets in understanding endothelial cell biology and vascular disease. The p47phox subunit of the NADPH oxidase can be an important regulator of certain Nox isoforms, including Nox1 and Nox2 which may be responsible for shear-induced superoxide production. In order to isolate p47phox-dependent shear responses, we took advantage of the p47phox-/- transgenic mouse model which lacks a functional p47phox subunit. We developed a method to isolate murine aortic endothelial cells using an enzymatic digestion technique. These cells expressed characteristic endothelial markers, including VE-cadherin, PECAM1, and eNOS, and aligned in the direction of flow. We successfully isolated primary murine aortic endothelial cells from both wild-type C57BL/6 mice (MAE-WT) and p47phox-/- mice (MAE-p47). Furthermore, we established an immortalized cell line from each of these cell types, iMAE-WT and iMAE-p47. We carried out microarray studies using Affymetrix Mouse Genome 430 2.0 Arrays (39,000+ transcripts) on MAE-WT and MAE-p47 that were exposed to atheroprotective LS or atherogenic OS for 24 hours. In comparison to LS, OS significantly changed the expression of 187 and 298 genes in MAE-WT and MAE-p47, respectively. Of those, 23 genes showed similar gene expression patterns in both cell types while 462 genes showed different gene expression patterns in the two cell types, demonstrating a considerable role for p47phox-based NADPH oxidases in shear-dependent gene expression. Changes in expression of several genes, including Kruppel-like factor 2 (Klf2), endothelial nitric oxide synthase (eNOS), angiopoietin 2 (Ang2), junctional adhesion molecule 2 (Jam2), bone morphogenic receptor type II (Bmpr2), and bone morphogenic protein 4 (Bmp4) were confirmed by quantitative PCR and/or immunoblotting using both primary cells and immortalized cells. Of these genes, our data suggest that Jam2, Bmpr2, and Bmp4 may be shear-sensitive in a p47phox-dependent manner. Taken together, our studies have identified a set of shear- and p47phox-sensitive genes, including unexpected and novel targets, which may play critical roles in vascular cell biology and pathobiology. Advisors/Committee Members: Jo, Hanjoong (Committee Chair), Griendling, Kathy (Committee Member), Harrison, David (Committee Member), Wang, May (Committee Member), Yoganathan, Ajit (Committee Member).

Subjects/Keywords: Endothelial cell; P47phox; NADPH oxidase; Microarray; Shear stress; Atherosclerosis; NAD (Coenzyme); Oxidases; Shear flow; Endothelium

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

APA (6^th Edition):

Sykes, M. C. (2008). Regulation of endothelial gene transcription by shear stress in a manner dependent on p47phox-based NADPH oxidases. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/24824

Chicago Manual of Style (16^th Edition):

Sykes, Michelle Christine. “Regulation of endothelial gene transcription by shear stress in a manner dependent on p47phox-based NADPH oxidases.” 2008. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/24824.

MLA Handbook (7^th Edition):

Sykes, Michelle Christine. “Regulation of endothelial gene transcription by shear stress in a manner dependent on p47phox-based NADPH oxidases.” 2008. Web. 16 Apr 2021.

Vancouver:

Sykes MC. Regulation of endothelial gene transcription by shear stress in a manner dependent on p47phox-based NADPH oxidases. [Internet] [Doctoral dissertation]. Georgia Tech; 2008. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/24824.

Council of Science Editors:

Sykes MC. Regulation of endothelial gene transcription by shear stress in a manner dependent on p47phox-based NADPH oxidases. [Doctoral Dissertation]. Georgia Tech; 2008. Available from: http://hdl.handle.net/1853/24824

Georgia Tech

27. Tolentino, Timothy P. The Roles of Membrane Rafts in CD32A Mediated Formation of a Phagocytic Contact Area.

Degree: PhD, Biomedical Engineering, 2007, Georgia Tech

URL: http://hdl.handle.net/1853/16127

► Membrane rafts are highly dynamic heterogeneous sterol- and sphingolipid-rich micro-domains on cell surfaces. They are generally believed to provide residency for cell surface molecules (e.g.,… (more)

▼ Membrane rafts are highly dynamic heterogeneous sterol- and sphingolipid-rich micro-domains on cell surfaces. They are generally believed to provide residency for cell surface molecules (e.g., adhesion and signaling molecules) and scaffolding to facilitate the functions of these molecules such as membrane trafficking, receptor transport, cell signaling, and endocytosis. Using laser scanning confocal microscopy and reflection interference microscopy (RIM), we studied the spatial and temporal distributions of membrane rafts and surface receptors, signaling molecules, and cell organelles during the formation of phagocytic contact areas. K562 cells, which naturally express CD32A, a cell surface receptor for the Fc portion of Immuno-globulin g (IgG), was chosen as a model for neutrophils. An opsonized target was modeled using a glass supported lipid bilayer reconstituted with IgG. CD32A was found to cluster and co-localize with membrane rafts. Placing the K562 cells on the lipid bilayer triggered a process of contact area formation that includes binding between receptors and ligands, their recruitment to the contact area, a concurrent membrane raft movement to and concentration in the contact area, and transport of CD32A, IgG, and membrane rafts to the Golgi complex. Characterization of these processes was performed using agents known to disrupt detergent resistant membranes (DRMs), dissolve actin microfilaments, and inhibit myosin motor activity, which abolished the CD32A clusters and prevented the contact area formation. The relevance to phagocytosis of contact area formation between K562 cells and lipid bilayers was demonstrated using micro-beads coated with a lipid bilayer reconstituted with IgG as the opsonized target instead of the glass supported planar lipid bilayer. Disruption of membrane rafts, salvation of the actin cytoskeleton, and inhibition of myosin II activity were found to inhibit phagocytosis. Here we have provided evidence that membrane rafts serve as platforms that are used to pre-cluster CD32A and transport CD32A along the actin cytoskeleton to the site of phagocytic synapse formation, followed by internalization to the Golgi complex. Advisors/Committee Members: Zhu, Cheng (Committee Chair), Dustin,Mike (Committee Member), Garcia, Andres (Committee Member), Jo, Hanjoong (Committee Member), Selvaraj, Periasamy (Committee Member).

Subjects/Keywords: Receptor-ligand binding; FcγRIIA; Phagocytosis; Signaling; Receptor-ligand complexes; Membrane lipids; Immune response; Cellular signal transduction; Cell membranes

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

APA (6^th Edition):

Tolentino, T. P. (2007). The Roles of Membrane Rafts in CD32A Mediated Formation of a Phagocytic Contact Area. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/16127

Chicago Manual of Style (16^th Edition):

Tolentino, Timothy P. “The Roles of Membrane Rafts in CD32A Mediated Formation of a Phagocytic Contact Area.” 2007. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/16127.

MLA Handbook (7^th Edition):

Tolentino, Timothy P. “The Roles of Membrane Rafts in CD32A Mediated Formation of a Phagocytic Contact Area.” 2007. Web. 16 Apr 2021.

Vancouver:

Tolentino TP. The Roles of Membrane Rafts in CD32A Mediated Formation of a Phagocytic Contact Area. [Internet] [Doctoral dissertation]. Georgia Tech; 2007. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/16127.

Council of Science Editors:

Tolentino TP. The Roles of Membrane Rafts in CD32A Mediated Formation of a Phagocytic Contact Area. [Doctoral Dissertation]. Georgia Tech; 2007. Available from: http://hdl.handle.net/1853/16127

Georgia Tech

28. Ni, Chih-Wen. Discovery of mechanosensitive microrna and messenger RNA in mouse arterial endothelium and in cultured endothelial cells.

Degree: PhD, Biomedical Engineering, 2010, Georgia Tech

URL: http://hdl.handle.net/1853/34674

► Atherosclerosis is a major contributor to cardiovascular disease and accounts for an estimated one third of deaths overall. In order to address the hemodynamic components… (more)

▼ Atherosclerosis is a major contributor to cardiovascular disease and accounts for an estimated one third of deaths overall. In order to address the hemodynamic components of disease pathogenesis, researchers have focused on mechanotransduction of flow-dependent shear stress in the vascular endothelium as a source of novel pathological mechanisms. Understanding how unidirectional, laminar blood flow protects vessels from atherogenesis, while disturbed, oscillatory blood flow promotes it, stands to provide enormous insight into disease pathogenesis and may provide powerful, specific new therapies for cardiovascular disease intervention. The overall objective of this dissertation was to determine which microRNAs (miRNAs) and mRNAs are regulated by different flow conditions in vascular endothelial cells in vitro and in mouse carotid artery endothelium in vivo, and to identify which miRNAs mediate flow-dependent vascular inflammation. The overall hypothesis of this project was that oscillatory shear (OS) and laminar shear (LS) stress differentially alter the expression of mechanosensitive miRNAs each capable of regulating complex networks of gene expression, which in turn leads to inflammation in endothelial cells. This hypothesis was tested using both in vitro and in vivo approaches, high throughput microarray analyses, and functional validation of specific targets by PCR. The findings from the partial carotid ligation model show that acute exposure to disturbed flow results in accelerated endothelial dysfunction and atherosclerosis in vivo. High-throughput microarrays reveal distinct expression profiles of both miRNAs and mRNAs in mouse endothelium exposed to disturbed flow suggesting the regulatory mechanisms by which miRNAs regulate mRNAs resulting in EC inflammation, the earliest stage of atherosclerosis. This in vivo study provides new insight into the mechanisms of flow induced atherosclerosis. In particular, the upregulation of miR-663 due to OS in HUVEC causes monocyte adhesion, but not endothelial apoptosis, in an ICAM-1 dependent manner. miR-663 regulates a group of genes including transcriptional factors and inflammatory genes which may also mediate OS-induced EC inflammation. Collectively, revealing the profiles of miRNAs and mRNAs regulated by hemodynamic flow provides a better understanding in vascular diseases and provide potential target for developing effective preventative therapeutic approaches in cardiovascular diseases. Advisors/Committee Members: Jo, Hanjoong (Committee Chair), Harrison, David (Committee Member), Griendling, Kathy (Committee Member), McIntire, Larry (Committee Member), Taylor, Robert (Committee Member).

Subjects/Keywords: MiRNA; IMAEC; Atherosclerosis; Shear stress; Endothelial cell; Endothelium; Vascular endothelium; Cardiovascular system Diseases; Cardiovascular system Diseases Diagnosis

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

APA (6^th Edition):

Ni, C. (2010). Discovery of mechanosensitive microrna and messenger RNA in mouse arterial endothelium and in cultured endothelial cells. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/34674

Chicago Manual of Style (16^th Edition):

Ni, Chih-Wen. “Discovery of mechanosensitive microrna and messenger RNA in mouse arterial endothelium and in cultured endothelial cells.” 2010. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/34674.

MLA Handbook (7^th Edition):

Ni, Chih-Wen. “Discovery of mechanosensitive microrna and messenger RNA in mouse arterial endothelium and in cultured endothelial cells.” 2010. Web. 16 Apr 2021.

Vancouver:

Ni C. Discovery of mechanosensitive microrna and messenger RNA in mouse arterial endothelium and in cultured endothelial cells. [Internet] [Doctoral dissertation]. Georgia Tech; 2010. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/34674.

Council of Science Editors:

Ni C. Discovery of mechanosensitive microrna and messenger RNA in mouse arterial endothelium and in cultured endothelial cells. [Doctoral Dissertation]. Georgia Tech; 2010. Available from: http://hdl.handle.net/1853/34674

Georgia Tech

29. Huang, Jun. A kinetic study of the T cell recognition mechanism.

Degree: PhD, Biomedical Engineering, 2008, Georgia Tech

URL: http://hdl.handle.net/1853/26693

► The mechanism of T cell recognition is the central but unsolved puzzle of adaptive immunology. The difficulties come from the multichain structure of TCR/CD3, the… (more)

▼ The mechanism of T cell recognition is the central but unsolved puzzle of adaptive immunology. The difficulties come from the multichain structure of TCR/CD3, the binate binding structure of the pMHC molecule, the diversity of the peptides presented on the APC, the critical role of coreceptor CD4/8, the communication between TCR and coreceptor CD4/8, the complex environment of interactions taking place and the binding and signaling coupled process of recognition. Most studies were using the 3D kinetic measurements or biological functional assays to address the mechanism of the T cell recognition. However, those assays are usually either lacking of physiology relevance or missing of the initial recognition signals. Here a 2D micropipette adhesion assay with high temporal resolution (-second) was used to address the in situ kinetics of molecular interaction at the membrane of live T cells. The aim of this project is to advance our understanding to the T cell recognition mechanism. The micropipette adhesion assay was firstly used to address a simple case, the resting state pMHC-CD8 interaction. In the absence of TCR-pMHC interaction, the pMHC-CD8 interaction has a very low affinity that depends on the MHC alleles and the lipid rafts of the T cell membrane where CD8 resides, but not on the peptide complexed to the MHC and whether the CD8 is an a a homodimer or an αβ heterodimer. For cognate pMHC, following the initial observation in the F5 T cell system, the binding also displays a two-step curve in the OTI T cell system. The first-step binding occurs before one second and has a very fast on-rate and off-rate (>2s ⁻¹), and the secondstep binding follows immediately but reaches a much higher level of binding. It was identified that the first-step binding is mediated by the TCR-pMHC interaction, and the second-step binding is triggered by the TCR-pMHC interaction but mediated by CD8- pMHC binding. The two-step binding is the unique property of cognate pMHC, and it can be abolished by disrupting the lipid rafts, inhibiting the Src family protein tyrosine kinases (PTK) or protein tyrosine phosphatase (PTP). The finding of two-step binding identifies a CD8-dependent signaling amplification pathway. The data also indicated the active communication between TCR and CD8 in the antigen recognition. The crosstalk between TCR and CD8 was further dissected using two anti-CD8 antibodies 53.6.7 and CT-CD8a. 53-6.7 can significantly enhance the binding of pMHC to the T cell. Although the enhancement is directly mediated by MHC-CD8 interaction, the enhancing role of this antibody is TCR dependent. Blocking the TCR-pMHC interaction on OTI T cell or expressing CD8 alone on a hybridoma abolished the enhancement. The enhancement is also dependent on the integrity of lipid rafts and the normal function of PTP. In contrast, the antibody CT-CD8 can inhibit the binding of pMHC to the T cells and interfere with the TCR-pMHC interaction. The enhancing or inhibitory role of these two anti-CD8 antibodies is reversely correlated with the affinities… Advisors/Committee Members: Zhu, Cheng (Committee Chair), Babensee, Julia (Committee Member), Dustin, Michael (Committee Member), Evavold, Brian (Committee Member), Jo, Hanjoong (Committee Member).

Subjects/Keywords: Recognition; CD8; TCR; PMHC; T cells; Cellular recognition

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

APA (6^th Edition):

Huang, J. (2008). A kinetic study of the T cell recognition mechanism. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/26693

Chicago Manual of Style (16^th Edition):

Huang, Jun. “A kinetic study of the T cell recognition mechanism.” 2008. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/26693.

MLA Handbook (7^th Edition):

Huang, Jun. “A kinetic study of the T cell recognition mechanism.” 2008. Web. 16 Apr 2021.

Vancouver:

Huang J. A kinetic study of the T cell recognition mechanism. [Internet] [Doctoral dissertation]. Georgia Tech; 2008. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/26693.

Council of Science Editors:

Huang J. A kinetic study of the T cell recognition mechanism. [Doctoral Dissertation]. Georgia Tech; 2008. Available from: http://hdl.handle.net/1853/26693

Georgia Tech

30. Butcher, Jonathan Talbot. The Effects of Steady Laminar Shear Stress on Aortic Valve Cell Biology.

Degree: PhD, Mechanical Engineering, 2004, Georgia Tech

URL: http://hdl.handle.net/1853/4824

► Aortic valve disease (AVD) affects millions of people of all ages around the world. Current treatment for AVD consists of valvular replacement with a non-living… (more)

▼ Aortic valve disease (AVD) affects millions of people of all ages around the world. Current treatment for AVD consists of valvular replacement with a non-living prosthetic valve, which is incapable of growth, self-repair, or remodeling. While tissue engineering has great promise to develop a living heart valve alternative, success in animal models has been limited. This may be attributed to the fact that understanding of valvular cell biology has not kept pace with advances in biomaterial development. Aortic valve leaflets are exposed to a complex and dynamic mechanical environment unlike any in the vasculature, and it is likely that native endothelial and interstitial cells respond to mechanical forces differently from other vascular cells. The objective of this thesis was to compare valvular cell phenotype to vascular cell phenotype, and assess the influence of steady shear stress on valvular cell biology. This thesis demonstrates that valvular endothelial cells respond differently to shear than vascular endothelial cells, by aligning perpendicular to the direction of steady shear stress, and by the differential regulation of hundreds of genes in both static and fluid flow environments. Valvular interstitial cells expressed a combination of contractile and synthetic phenotypes not mimicked by vascular smooth muscle cells. Two three-dimensional leaflet models were developed to assess cellular interactions and the influences of steady laminar shear stress. Valvular co-culture models exhibited a physiological response profile, while interstitial cell-only constructs behaved more pathologically. Steady shear stress enhanced physiological functions of valvular co-cultures, but increased pathological response of interstitial cell-only constructs. These results showed that valvular cells, whether cultured separately or together, behaved distinctly different from vascular cells. It was also determined that shear stress alone cannot induce tissue remodeling to more resemble native valve leaflets. The leaflet models developed in this thesis can be used in future experiments to explore valvular cell biology, assess the progression of certain forms AVD, and develop targeted diagnostic and therapeutic strategies to hopefully eliminate the need for valvular replacement entirely. Advisors/Committee Members: Nerem, Robert M (Committee Chair), Garcia, Andres (Committee Member), Hilbert, Stephen L (Committee Member), Jo, Hanjoong (Committee Member), Yoganathan, Ajit P (Committee Member).

Subjects/Keywords: Microarray; Interstitial cells; Aortic valve; Shear stress; Endothelial cells

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APA (6^th Edition):

Butcher, J. T. (2004). The Effects of Steady Laminar Shear Stress on Aortic Valve Cell Biology. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/4824

Chicago Manual of Style (16^th Edition):

Butcher, Jonathan Talbot. “The Effects of Steady Laminar Shear Stress on Aortic Valve Cell Biology.” 2004. Doctoral Dissertation, Georgia Tech. Accessed April 16, 2021. http://hdl.handle.net/1853/4824.

MLA Handbook (7^th Edition):

Butcher, Jonathan Talbot. “The Effects of Steady Laminar Shear Stress on Aortic Valve Cell Biology.” 2004. Web. 16 Apr 2021.

Vancouver:

Butcher JT. The Effects of Steady Laminar Shear Stress on Aortic Valve Cell Biology. [Internet] [Doctoral dissertation]. Georgia Tech; 2004. [cited 2021 Apr 16]. Available from: http://hdl.handle.net/1853/4824.

Council of Science Editors:

Butcher JT. The Effects of Steady Laminar Shear Stress on Aortic Valve Cell Biology. [Doctoral Dissertation]. Georgia Tech; 2004. Available from: http://hdl.handle.net/1853/4824

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