The Cellular Repressor Of E1A-stimulated Genes Promotion Of Human Vascular Smooth Muscle Cells Differentiation In Vitro

Background and Objective Smooth muscle cells (SMCs) in the adult artery wall can manifest a diversity of phenotypes. The quiescent, fully differentiated phenotype characterizes the usual state in the vascular wall responsible for vascular contraction and dilation. The migratory or proliferative phenotype is present during SMCs response to injury. Accordingly, the phenotypic modulation of vascular smooth muscle cells (VSMCs) from the differentiated state (contractile phenotype) to the dedifferentiated one (synthetic phenotype) is an essential process involved in the development and progression of restenosis after angioplasty or stent application as well as atherosclerosis. Once VSMCs undergo phenotypic switching, they can migrate from the media toward the intima, and obtain the ability of proliferation. Although many transcriptional factors, growth factors and cytokines have been reported to regulate differentiation, proliferation and migration of VSMCs, the mainly mechanisms of regulation the VSMCs differentiation and phenotype modulation, however, remain unclear because that overall regulation of SMCs differentiation and its responses to the changing local environmental cues, is extremely complex and involves the cooperative interaction of many factors and signaling pathways.CREG, the Cellular Repressor of E1A-stimulate Genes, have been previously reported as a transcriptional regulator that antagonizes E2F-dependent transcriptional activation and the oncogenic transformation of primary cells by the Adenovirus E1A oncoprotein to cooperate with the...