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You searched for +publisher:"University of North Carolina" +contributor:("Majesky, Mark W."). Showing records 1 – 3 of 3 total matches.

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University of North Carolina

1. Hoglund, Virginia J. Characterization of the Arterial Adventitia as a Sonic Hedgehog Responsive Niche.

Degree: 2012, University of North Carolina

While formerly viewed as merely connective tissue, the emerging view of the arterial adventitia is that of a complex and organized vascular progenitor cell niche. Previously, our lab has identified a domain of Sonic Hedgehog (Shh) signaling restricted to the adventitia. This domain is locally produced and maintained, with the peak of activity being during embryonic and neonatal development of the vessel from embryonic day 14.5 (e14.5) to postnatal day 14 in the mouse. Developmental studies suggest that the mesenchyme continuous with the perichondrium of the axial skeleton contains Shh responsive cells that may contribute to adventitial development around e14.5. The cell types that participate in this Sonic Hedgehog adventitial signaling community are CD68-positive macrophages, Sca1-positive progenitor cells, and Perilipin A-positive adipocytes that make and/or respond to Shh protein as shown using transgenic reporter mice. Thus, we characterize the adventitia as a Shh responsive vascular niche. Advisors/Committee Members: Hoglund, Virginia J., Majesky, Mark W..

Subjects/Keywords: School of Medicine; Curriculum in Genetics and Molecular Biology

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

APA (6th Edition):

Hoglund, V. J. (2012). Characterization of the Arterial Adventitia as a Sonic Hedgehog Responsive Niche. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:b9dc92aa-4bd4-4770-9ffa-1a5f0340b3fd

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):

Hoglund, Virginia J. “Characterization of the Arterial Adventitia as a Sonic Hedgehog Responsive Niche.” 2012. Thesis, University of North Carolina. Accessed November 27, 2020. https://cdr.lib.unc.edu/record/uuid:b9dc92aa-4bd4-4770-9ffa-1a5f0340b3fd.

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

MLA Handbook (7th Edition):

Hoglund, Virginia J. “Characterization of the Arterial Adventitia as a Sonic Hedgehog Responsive Niche.” 2012. Web. 27 Nov 2020.

Vancouver:

Hoglund VJ. Characterization of the Arterial Adventitia as a Sonic Hedgehog Responsive Niche. [Internet] [Thesis]. University of North Carolina; 2012. [cited 2020 Nov 27]. Available from: https://cdr.lib.unc.edu/record/uuid:b9dc92aa-4bd4-4770-9ffa-1a5f0340b3fd.

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

Council of Science Editors:

Hoglund VJ. Characterization of the Arterial Adventitia as a Sonic Hedgehog Responsive Niche. [Thesis]. University of North Carolina; 2012. Available from: https://cdr.lib.unc.edu/record/uuid:b9dc92aa-4bd4-4770-9ffa-1a5f0340b3fd

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


University of North Carolina

2. Regan, Jenna Nicole. Regulation of adventitia-resident progenitor cells.

Degree: 2010, University of North Carolina

Far from the inert structural component that was the prevailing view for many years, the arterial adventitia is a region of active signaling that harbors Sca1+ vascular progenitor cells as well as many other cell types. We have shown that a sonic hedgehog (Shh) signaling domain is restricted to the adventitial layer of artery wall beginning at embryonic day 15.5. Hedgehog (Hh)-responsive cells, colocalize with a circumferential ring of Shh protein concentrated between the media and adventitia. Furthermore, Sca1+ progenitor cells (AdvSca1 cells) reside within the Hh signaling domain and are reduced in number in Shh-/- mice. As a population, AdvSca1 cells express transcription factors thought to be required for smooth muscle cell (SMC) differentiation, including serum response factor (SRF) and myocardin family members, yet the cells do not express SMC marker proteins in vivo. However, upon removal of AdvSca1 cells from the adventitial environment, they readily differentiate to SMC-like cells in vitro. Repression of SRF-dependent transcription may be mediated by SRF co-repressors such as Klf4, Msx1, and FoxO4, all of which are expressed by AdvSca1 cells in vivo. Knockdown of Klf4 in AdvSca1 cells in vitro results in extensive down-regulation of Sca1 and defects in Sca1+ cell proliferation. In vitro and in vivo experiments have shown that AdvSca1 cells possess the potential for SMC, pericyte/mural cell, adipogenic, ostogenic, endothelial, and macrophage differentiation. Thus, AdvSca1 cells are regulated, in part, by Hh signaling and the transcription factor Klf4 and function as progenitors for multiple cell types with physiological and pathological relevance to the artery wall. Advisors/Committee Members: Regan, Jenna Nicole, Majesky, Mark W., University of North Carolina at Chapel Hill.

Subjects/Keywords: School of Medicine; Curriculum in Genetics and Molecular Biology

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

APA (6th Edition):

Regan, J. N. (2010). Regulation of adventitia-resident progenitor cells. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:a3e93b07-767c-47fb-8ba2-22d420f95f31

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):

Regan, Jenna Nicole. “Regulation of adventitia-resident progenitor cells.” 2010. Thesis, University of North Carolina. Accessed November 27, 2020. https://cdr.lib.unc.edu/record/uuid:a3e93b07-767c-47fb-8ba2-22d420f95f31.

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

MLA Handbook (7th Edition):

Regan, Jenna Nicole. “Regulation of adventitia-resident progenitor cells.” 2010. Web. 27 Nov 2020.

Vancouver:

Regan JN. Regulation of adventitia-resident progenitor cells. [Internet] [Thesis]. University of North Carolina; 2010. [cited 2020 Nov 27]. Available from: https://cdr.lib.unc.edu/record/uuid:a3e93b07-767c-47fb-8ba2-22d420f95f31.

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

Council of Science Editors:

Regan JN. Regulation of adventitia-resident progenitor cells. [Thesis]. University of North Carolina; 2010. Available from: https://cdr.lib.unc.edu/record/uuid:a3e93b07-767c-47fb-8ba2-22d420f95f31

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


University of North Carolina

3. Callis, Thomas. THE REGULATION OF GENE EXPRESSION DURING HEART DEVELOPMENT AND DISEASE.

Degree: Cell Biology and Physiology, 2008, University of North Carolina

Cardiovascular disease remains one of the most common fatal and disabling disorders in the United States. The development of the heart and pathological processes leading to heart disease are intimately linked to the regulation of gene expression. By understanding the complex genetic and molecular pathways controlling cardiac gene expression, new therapies might be developed for the prevention and treatment of heart disease. My research has focused upon the fundamental mechanisms of transcriptional and post-transcriptional regulation of gene expression. In particular, I have investigated how transcription factors and microRNAs (miRNAs) coordinate cardiac gene expression during development and in disease. Myocardin is a cardiac and smooth muscle-specific transcriptional cofactor for serum response factor (SRF). Myocardin potently activates target gene expression by tethering with SRF bound to SRF-responsive elements. However the upstream signaling pathways controlling myocardin activity and specificity were unknown. Bone Morphogenetic Proteins (BMPs) play important roles in cardiovascular development and I find that Smad1, an effector of the BMP signaling pathway, synergistically activates myocardin-dependent cardiac gene expression. This discovery that myocardin participates in a BMP signaling-dependent cardiac gene transcriptional program helps address how myocardin transactivation of cardiac versus smooth muscle genes is controlled. Much of the current understanding of the genetic pathways controlling cardiac gene expression is based upon studies of transcription factors and regulatory enhancer sequences required for cardiac gene transcription. The discovery of miRNAs has further increased this complexity by adding another layer of regulation at the post-transcriptional level. I show that the miR-208 family, miR-208a and miR-208b, are differentially expressed during heart development, paralleling the expression of their respective host genes alpha- and beta-myosin heavy chain (αMHC and βMHC). Using genetically engineered mice that overproduce miR-208a specifically in the heart or lack miR-208a altogether, I show that miR-208a is an important regulator of cardiac hypertrophy and cardiac conduction. Collectively, my studies of the transcription factor myocardin and the miR-208 family extend the current understanding of how cardiac gene expression is regulated during heart development and disease. Advisors/Committee Members: Callis, Thomas, Wang, Da-Zhi, Bankaitis, Vytas A., Majesky, Mark W., Hammond, Scott, Conlon, Frank, Beckers, Con.

Subjects/Keywords: School of Medicine; Department of Cell Biology and Physiology

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

APA (6th Edition):

Callis, T. (2008). THE REGULATION OF GENE EXPRESSION DURING HEART DEVELOPMENT AND DISEASE. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:6a1f3325-a0ae-45a9-80e2-ce653fd5526f

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):

Callis, Thomas. “THE REGULATION OF GENE EXPRESSION DURING HEART DEVELOPMENT AND DISEASE.” 2008. Thesis, University of North Carolina. Accessed November 27, 2020. https://cdr.lib.unc.edu/record/uuid:6a1f3325-a0ae-45a9-80e2-ce653fd5526f.

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

MLA Handbook (7th Edition):

Callis, Thomas. “THE REGULATION OF GENE EXPRESSION DURING HEART DEVELOPMENT AND DISEASE.” 2008. Web. 27 Nov 2020.

Vancouver:

Callis T. THE REGULATION OF GENE EXPRESSION DURING HEART DEVELOPMENT AND DISEASE. [Internet] [Thesis]. University of North Carolina; 2008. [cited 2020 Nov 27]. Available from: https://cdr.lib.unc.edu/record/uuid:6a1f3325-a0ae-45a9-80e2-ce653fd5526f.

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

Council of Science Editors:

Callis T. THE REGULATION OF GENE EXPRESSION DURING HEART DEVELOPMENT AND DISEASE. [Thesis]. University of North Carolina; 2008. Available from: https://cdr.lib.unc.edu/record/uuid:6a1f3325-a0ae-45a9-80e2-ce653fd5526f

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

.