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Is Myocyte-derived VEGF In Adult Mice Required For Normal Skeletal ...
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Ts for the Doctor of Philosophy in Biomedical Sciences by Amy Elizabeth Knapp Committee in Charge: Professor Michael C. Hogan, Chair Professor Peter D. Wagner, Co-Chair Professor Randall R. Johnson Professor Richard L. Lieber Professor Nicholas J. Webster 2009 UMI Number: 3360169 INFORMATION TO USERS The quality of this reproduction is dependent upon the quality of the copy submitted. Broken or indistinct print, colored or poor quality illustrations and photographs, print bleed-through.
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Contractile FAQ
Vascular endothelial growth factor-A (VEGF) is one of the most important growth factors for regulation of vascular development and angiogenesis. Since bone is a highly vascularized organ and angiogenesis plays an important role in osteogenesis, VEGF also influences skeletal development and postnatal bone repair.
VEGF promotes the growth of myogenic fibers and protects myogenic cells from apoptosis. The above-reported observations suggest that, in addition to its well-documented angiogenic properties, VEGF might also exert a direct effect on muscle fibers.
A myocyte (also known as a muscle cell) is the type of cell found in some types of muscle tissue. Myocytes develop from myoblasts to form muscles in a process known as myogenesis. There are two specialized forms of myocytes with distinct properties: cardiac, and smooth muscle cells.
Studies have shown that VEGF acts as an anti-apoptotic factor, protecting hematopoietic cells from programmed cell death. Both VEGF and VEGFR-2 are expressed in normal hematopoietic cells and in leukemic cells, and VEGF suppresses apoptosis induced by ionizing irradiation in both cell types.
Vascular endothelial growth factor (VEGF) expression is enhanced in ischemic skeletal muscle and is thought to play a key role in the angiogenic response to ischemia. However, it is still unknown whether, in addition to new blood vessel growth, VEGF modulates skeletal muscle cell function.
VEGF gene polymorphisms regulate human retinal vascular endothelial cell proliferation and apoptosis through ASF/SF2-associated alternative splicing. [Association of polymorphisms of VEGF and VEGFR1 pathways related genes and risk of pre-eclampsia].
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