YY1 directly interacts with myocardin to repress the triad myocardin/SRF/CArG box-mediated smooth muscle gene transcription during smooth muscle phenotypic modulation.

摘要: Yin Yang 1 (YY1) regulates gene transcription in a variety of biological processes. In this study, we aim to determine the role YY1 vascular smooth muscle cell (VSMC) phenotypic modulation both vivo and vitro. Here show that injury rodent carotid arteries induces expression along with reduced differentiation markers carotids. Consistent finding, is induced differentiated VSMCs response serum stimulation. To underlying molecular mechanisms, found suppresses CArG box-dependent SMC-specific genes including SM22α, SMα-actin SMMHC. Interestingly, transcriptional activity SM22α promoter by hindering binding factor (SRF) proximal box. also transactivation myocardin (MYOCD), master regulator for SRF form MYOCD/SRF/CArG box triad (known as the ternary complex). Mechanistically, directly interacts MYOCD competitively displace from SRF. This first evidence showing inhibits SMC targeting MYOCD. These findings provide new mechanistic insights into regulatory mechanisms govern pathogenesis diseases.