Myocardin the phenotype of vascular smooth muscle cells in the mechanism of transformation.doc
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Myocardin the phenotype of vascular smooth muscle cells in the mechanism of transformation
PAGE \* MERGEFORMAT 14
Myocardin the phenotype of vascular smooth muscle cells in the mechanism of transformation
[Abstract] Objective To investigate the Myocardin in vascular smooth muscle cells (VSMC) Phenotypic mechanism of action. Methods Cell Transfection Method to exogenous Myocardin and SRF in cultured VSMC in the over-expression, application RT PCR, Western blot and modified Coomassie brilliant blue staining used to detect the transfected VSMC contraction type-specific marker gene expression and structural changes in the cytoskeleton. results when containing the gene encoding SRF and Myocardin expression plasmid transfected into cultured VSMC common when the contractile VSMC marker genes SM22 @ and SM @ actin mRNA and protein of a significant increase, but also to promote VSMC cytoskeleton reconstruction. and cultured VSMC Dandu transferred or Myocardin expression of transfected SRF plasmids, related indexes did not change. conclusions, Endogenous Expression of Myocardin and SRF can promote VSMC mandatory specific marker gene expression and cytoskeleton remodeling, which is proliferation of VSMC induced into the stationary phase transformation to shrink.
[Keywords:] Myocardin; serum response factors; of vascular smooth muscle cell; Phenotypic
Vascular smooth muscle cells (VSMC) phenotype in a variety of development and progression of cardiovascular disease, studies have shown that serum response factors (SRF) its cis-element CArG (CC (A / T) 6GG) box is the start VSMC interaction The core mechanism of specific gene expression (1). However, CArG components is not unique to VSMC-specific gene, is widely found in smooth muscle, cardiac muscle, skeletal muscle and some non-muscle cells. Therefore, with the SRF CArG interactions alone are difficult to explain cell-specific gene expression. Myocardin is a nuclear protein found in 2001, SAP domain family member (2), in a variety of non-muscle cells, SRF-dependent manner to start the muscle-specific g
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