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You searched for +publisher:"University of North Carolina" +contributor:("Wang, Da-Zhi"). Showing records 1 – 2 of 2 total matches.

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University of North Carolina

1. Chen, Jianfu. MicroRNA function in muscle development.

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

MicroRNAs (miRNAs) are a class of non-coding RNAs of [approximately]22 nucleotides in length that post-transcriptionally regulate gene expression. While there are more than 600 miRNAs identified in human genome, the biological functions of miRNAs are largely unknown. Here we show that microRNA-1 (miR-1) and microRNA-133 (miR-133) are specifically expressed in cardiac and skeletal muscle. Paradoxically, miR-1 and miR-133 exert opposing effects during skeletal muscle development in vitro and in vivo. miR-1 promotes myogenesis by targeting histone deacetylase 4 (HDAC4), a signal dependent chromatin regulator that represses MEF2 activity. MEF2, in turn, potently activates miR-1/-133 expression. In contrast, miR-133 enhances myoblast proliferation by repressing serum response factor (SRF), an essential regulator for muscle proliferation and differentiaiton. Together, these findings suggest that miR-1 and miR-133 are integrated into existing genetic circuits that control skeletal muscle development. We address the function of miRNAs during heart development using mouse genetic approaches. Cardiac-specific deletion of Dicer, a RNase III endonuclease responsible for miRNA maturation, leads to rapidly progressive dilated cardiomyopathy (DCM), heart failure, and postnatal lethality. Dicer mutant mice show misexpression of cardiac contractile proteins and profound sarcomere disarray. Functional analyses indicate significantly reduced heart rates and decreased fractional shortening of Dicer mutant hearts. Consistent with the role of Dicer in animal hearts, Dicer expression was decreased in end-stage human DCM and failing hearts and, most importantly, a significant increase of Dicer expression was observed in those hearts after left ventricle assist devices were inserted to improve cardiac function. Together, our studies demonstrate essential roles of Dicer in cardiac contraction and indicate that miRNAs play critical functions in normal cardiac development and function To examine the potential involvement of miRNAs in muscle stem cells, known as satellite cells, we examined miRNA expression profiles during satellite cell differentiation and skeletal muscle regeneration. miR-1 and its isoform, miR-206, are sharply up-regulated during satellite cell differentiation and down-regulated in muscle injury. miR-1 and -206 facilitate satellite cell differentiation by restricting satellite cell proliferative potential. We identify Pax7, an essential stem cell maintenance gene of satellite cells, as one of direct regulatory targets of miR-1 and -206. Knock down in vivo using antagomirs specifically against miR-1 and -206 in neonatal mouse skeletal muscle enhances satellite cell proliferation and Pax7 protein levels. Conversly, sustained Pax7 expression due to the loss of miR-1 and -206 repressive elements at Pax7 3' UTR inhibits myogenic progenitor differentiation. Our studies reveal a critical role of miR-1 and -206 in satellite cells and suggest that miRNAs participate in a regulatory circuit that allows rapid gene program transiton from… Advisors/Committee Members: Chen, Jianfu, Wang, Da-zhi.

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):

Chen, J. (2008). MicroRNA function in muscle development. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:0dd67c58-afee-42ce-b80c-2e648886589b

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):

Chen, Jianfu. “MicroRNA function in muscle development.” 2008. Thesis, University of North Carolina. Accessed November 27, 2020. https://cdr.lib.unc.edu/record/uuid:0dd67c58-afee-42ce-b80c-2e648886589b.

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

MLA Handbook (7th Edition):

Chen, Jianfu. “MicroRNA function in muscle development.” 2008. Web. 27 Nov 2020.

Vancouver:

Chen J. MicroRNA function in muscle development. [Internet] [Thesis]. University of North Carolina; 2008. [cited 2020 Nov 27]. Available from: https://cdr.lib.unc.edu/record/uuid:0dd67c58-afee-42ce-b80c-2e648886589b.

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

Council of Science Editors:

Chen J. MicroRNA function in muscle development. [Thesis]. University of North Carolina; 2008. Available from: https://cdr.lib.unc.edu/record/uuid:0dd67c58-afee-42ce-b80c-2e648886589b

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


University of North Carolina

2. 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

.