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You searched for +publisher:"University of Alabama – Birmingham" +contributor:("Rosa Serra"). Showing records 1 – 3 of 3 total matches.

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1. Ramaswamy, Girish. Regulation Of Paps Synthetase 2 By Tranforming Growth Factor-Beta And Its Role In The Maintenance Of Mouse Articular Cartilage.

Degree: 2012, University of Alabama – Birmingham

Articular cartilage is a special type of hyaline cartilage present at the end of long bones and facilitates smooth functioning of joints and transfer of load. While most cartilage elements in the body are transient, articular cartilage is permanent and functions throughout life. Osteoarthritis (OA) is a joint degenerative disease and the leading cause of disability in the industrialized world. A multitude of factors including aging, orthopedic trauma, genetics etc. have been associated with OA. Transforming growth factor-β (TGF-β) is a multifunctional polypeptide which plays an important role in chondrocyte proliferation, differentiation and synthesis of extracellular matrix. Previously, mice with dominant negative interference of TGF-β type II receptor (DNIIR) was shown to develop joint degeneration and exhibit human OA symptoms. Similar results were found in mice with other mutations in the TGF-β signaling pathway, but none of these studies characterized the biomechanical, biochemical and gene expression changes in the articular cartilage of these mutants. In order to fully understand the role of TGF-β in the maintenance of articular cartilage, we employed the DNIIR model in our studies. Biomechanical tests revealed a significant decrease in indentation stiffness in DNIIR articular cartilage as compared to wild type mice. From microarray of bovine articular chondrocytes cultured in micromass and treated/left untreated with TGF-β, we generated direct targets of TGF-β which included genes such as Papss2 and Plod2 that regulate global post-translational modifications of the extracellular matrix. As Papss2 is crucial for sulfation of cartilage glycosaminoglycans, we examined Papss2 expression and found marked reduction of Papss2 mRNA and protein in articular cartilage of DNIIR mice as compared to wild type. By immunofluorescence and Alcian Blue critical electrolyte staining we demonstrated that reduction in Papss2 led to a decrease in sulfation of cartilage matrix especially chondroitin-4-sulfate and upregulation of unsulfated chondroitin in the DNIIR mice with no change in aggrecan core protein. In support of TGF-&beta regulation of Papss2, we also show that Tgfbr2 homozygous null mice exhibit a severe decrease in Papss2 expression levels embryonically. Overall, we propose that TGF-β maintains the biomechanical integrity by regulating Papss2 and sulfation of glycosaminoglycans in mouse articular cartilage.

PhD

1 online resource (xi, 101 pages) :illustrations (some color)

Biomedical Engineering

UNRESTRICTED

Advisors/Committee Members: Rosa Serra, Eberhardt, Alan W. Murphy-Ullrich,Joanne Bellis, Susan L. Wick, Timothy M..

Subjects/Keywords: Articular cartilage – Diseases – Genetic aspects.<; br>; Osteoarthritis – Animal models.<; br>; Genetic regulation.<; br>; Enzymes – Regulation.<; br>; Oxygenases.<; br>; Ligases.<; br>; Transforming growth factors-beta.<; br>; Chondroitin sulfates.<; br>; DNA microarrays.

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

APA (6th Edition):

Ramaswamy, G. (2012). Regulation Of Paps Synthetase 2 By Tranforming Growth Factor-Beta And Its Role In The Maintenance Of Mouse Articular Cartilage. (Thesis). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1594

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

Chicago Manual of Style (16th Edition):

Ramaswamy, Girish. “Regulation Of Paps Synthetase 2 By Tranforming Growth Factor-Beta And Its Role In The Maintenance Of Mouse Articular Cartilage.” 2012. Thesis, University of Alabama – Birmingham. Accessed December 12, 2019. http://contentdm.mhsl.uab.edu/u?/etd,1594.

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

MLA Handbook (7th Edition):

Ramaswamy, Girish. “Regulation Of Paps Synthetase 2 By Tranforming Growth Factor-Beta And Its Role In The Maintenance Of Mouse Articular Cartilage.” 2012. Web. 12 Dec 2019.

Vancouver:

Ramaswamy G. Regulation Of Paps Synthetase 2 By Tranforming Growth Factor-Beta And Its Role In The Maintenance Of Mouse Articular Cartilage. [Internet] [Thesis]. University of Alabama – Birmingham; 2012. [cited 2019 Dec 12]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1594.

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

Council of Science Editors:

Ramaswamy G. Regulation Of Paps Synthetase 2 By Tranforming Growth Factor-Beta And Its Role In The Maintenance Of Mouse Articular Cartilage. [Thesis]. University of Alabama – Birmingham; 2012. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1594

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

2. Baxley, Sarah. The role of WNT5A in mammary gland development.

Degree: PhD, 2010, University of Alabama – Birmingham

Transforming growth factor {esc}gb {esc}s(TGF-{esc}gb{esc}s) negatively regulates mammary gland development and requires Wnt5a to exert some of these effects on mammary gland development. Wnt5a is a non-canonical signaling Wnt that is expressed in all stages of mammary gland development except lactation. Using slow release pellets containing Wnt5a, as well as Wnt5a null tissue, we previously showed that Wnt5a also acts to limit mammary development. Initial studies revealed a potential role for TGF-{esc}gb {esc}sand Wnt5a in regulating mammary gland progenitor cells, indicating they may act to regulate the stem and progenitor cell population. In order to study the role of Wnt5a on mammary stem and progenitor cell maintenance, we wanted to create a new mouse model. Here, we generated transgenic mice that overexpress Wnt5a in the mammary epithelium using the MMTV promoter (M5a mice). Lactation was impaired in two high Wnt5a expressing lines. Lactation defects could not be explained by differences in apoptosis, lineage differentiation, milk synthesis or secretion. Instead, Wnt5a overexpression led to a failure in oxytocin response and milk ejection, similar to mice with a mutation in Connexin43 (Cx43), we examined Cx43 phosphorylation and localization in M5a mice. In wild type mice, Cx43 switched from a phosphorylated to a more hypophosphorylated form after parturition. In contrast, Cx43 was maintained in the phosphorylated form after parturition in M5a mice. Similarly, mammary myoepithelial cells grown in culture and treated with Wnt5a exhibited altered Cx43 phosphorylation relative to vehicle treated control cells. We propose that Wnt5a inhibits the response to oxytocin and prevents milk ejection through regulation of Cx43 phosphorylation. Additionally, we examined the effects of Wnt5a and TGF-{esc}gb {esc}son mammary stem cell populations and found no direct, significant effects on stem cell number. Although Wnt5a and TGF-{esc}gb {esc}smay not regulate stem cell number, we hypothesize they may direct other aspects of stem or progenitor cell maintenance, such as progenitor proliferation or stem cell self-renewal. Overall, we conclude that Wnt5a and TGF-{esc}gb {esc}smay regulate the mammary progenitor cell population. Additionally, Wnt5a overexpression can alter mammary Cx43 phosphorylation at parturition, inhibiting the milk ejection response.

1 online resource (x, 85 pages) :illustrations

University of Alabama at Birmingham2010.

Cell Biology

Joint Health Sciences

UNRESTRICTED

Advisors/Committee Members: Rosa Serra, Anupam Agarwal<br>, Chenbei Chang<br>, Andra Frost<br>, Christopher Klug<br>, Jianbo Wang..

Subjects/Keywords: Breast Neoplasms<; br>; Lactation<; br>; Mammary Glands, Animal – metabolism<; br>; Mammary Neoplasms, Experimental – metabolism.<; br>; Transforming Growth Factor beta – metabolism<; br>; Wnt Proteins – metabolism.

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

APA (6th Edition):

Baxley, S. (2010). The role of WNT5A in mammary gland development. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1812

Chicago Manual of Style (16th Edition):

Baxley, Sarah. “The role of WNT5A in mammary gland development.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed December 12, 2019. http://contentdm.mhsl.uab.edu/u?/etd,1812.

MLA Handbook (7th Edition):

Baxley, Sarah. “The role of WNT5A in mammary gland development.” 2010. Web. 12 Dec 2019.

Vancouver:

Baxley S. The role of WNT5A in mammary gland development. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2019 Dec 12]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1812.

Council of Science Editors:

Baxley S. The role of WNT5A in mammary gland development. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1812

3. Cox, Megan Karen. Tgf-β And Erg In Intervertebral Disc Development.

Degree: 2013, University of Alabama – Birmingham

The intervertebral disc (IVD) is a fibrocartilaginous tissue that acts as a shock absorber between adjacent vertebrae in the spinal column. It is comprised of two parts, the inner jelly-like nucleus pulposus (NP) and the outer more fibrous annulus fibrosus (AF). Most IVD research has focused on the development of the NP, which is derived from condensations of the notochord involving sonic hedgehog (Shh) signaling. In contrast, very little is known about the molecular mechanisms underlying the specific development of the AF of the IVD. The AF is derived from the sclerotome, which is formed by the ventral half of the somites. It is yet to be determined what genes control this differentiation into IVD. The transforming growth factor-β (TGF-β) signaling pathway is important for various aspects of development. One of these developmental processes is the formation of the AF of the IVD. Our previous studies show that conditionally deleting the Tgf-β type II receptor (Tgfbr2) from type II collagen-expressing cells in mice, results in defective IVD development.This leads us to believe that TGF-β is involved in IVD development as well as its long-term maintenance. To elucidate the mechanism of action, we used microarrays to determine what genes were expressed in the IVD during development as well as which genes were dys-regulated by the deletion of TGF-β signaling in vivo or the addition of TGF-β in vitro. We confirmed the expression of many of these genes in the IVD and selected transcription factors for further study, including avian erythroblastosis virus E-26 (v-ets) oncogene related (ERG). While ERG was able to suppress markers of the vertebral body, it was unable to increase IVD markers by itself. However, in the presence of TGF-β1, ERG appears to be able to enhance the effect of TGF-β on IVD markers. This suggests that TGF-β may be acting to suppress the development of neighboring vertebral bodies, as well as induce the development of the AF through induction of ERG.

PhD

1 online resource (xi, 122 pages) :illustrations

Ph.D.University of Alabama at Birmingham2013.

Cell Biology

Medicine

annulus fibrosus, ERG, Intervertebral Disc, Tgfbeta

UNRESTRICTED

Advisors/Committee Members: Rosa Serra, Bellis,Susan Chang,Chenbei Javed,Amjad Jun,Ho-Wook.

Subjects/Keywords: Fibrocartilage – metabolism.<; /br>; Intervertebral Disc – anatomy & histology.<; /br>; Intervertebral Disc – embryology.<; /br>; Transcription Factors<; /br>; Transforming Growth Factor beta

…Philip Sohn, Megan Cox, Dongquan Chen, Rosa Serra BMC Developmental Biology Copyright 2010 by… 

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

APA (6th Edition):

Cox, M. K. (2013). Tgf-β And Erg In Intervertebral Disc Development. (Thesis). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1643

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

Chicago Manual of Style (16th Edition):

Cox, Megan Karen. “Tgf-β And Erg In Intervertebral Disc Development.” 2013. Thesis, University of Alabama – Birmingham. Accessed December 12, 2019. http://contentdm.mhsl.uab.edu/u?/etd,1643.

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

MLA Handbook (7th Edition):

Cox, Megan Karen. “Tgf-β And Erg In Intervertebral Disc Development.” 2013. Web. 12 Dec 2019.

Vancouver:

Cox MK. Tgf-β And Erg In Intervertebral Disc Development. [Internet] [Thesis]. University of Alabama – Birmingham; 2013. [cited 2019 Dec 12]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1643.

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

Council of Science Editors:

Cox MK. Tgf-β And Erg In Intervertebral Disc Development. [Thesis]. University of Alabama – Birmingham; 2013. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1643

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

.