Myocardin is a potent coactivator of SRF and expressed mainly in cardiomyocytes and smooth muscle cells (SMCs), Myocardin is important for SMC differentiation, but its precise role in regulating the initiation of SMC development is less clear. Constuction and function analysis of myocardin promoter luciferase reporter plasmid will provide the theory basis for researching the function of myocardin in SMC differentiation. In this study, a mouse myocardin promoter luciferase reporter construct was successfully constructed. To determine whether myocardin transcription activity were regulated by several factors, which play important roles in SMC differentiation, luciferase repoeter assays were performed in COS-7 cells and vascular smooth muscle cells (VSMCs). The results illustrated that Smad2 significantly activated myocardin promoter, but Smad3 signaling was inhibitory to myocardin expression at 18h. Myocardin promoter transactivity was inhibited by estrogen receptor α (ERα), and enhanced by p300. These findings indicated myocardin might be regulated by multi-signals and these factors might affect SMC differentiation through activating or inhibiting myocardin transcription.

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Abstract-Myocardin and associated transcription factor (Myocardin-Related Transcription Factors, MRTFs) by serum response factor (SRF) together constitute the composition of molecular differentiation of muscle cell switch. This paper focuses on the vascular smooth muscle cells (vascular smooth muscle cells, VSMCs), breast cancer cell lines MCF-7 and African green monkey kidney cell line COS-7 as the research object, using cellular and molecular biological methods to study the transcription factor Myocardin and Estrogen receptor α (ER α) in the regulation of differentiation of vascular smooth muscle cell function. The luciferase reporter assay in COS-7 and MCF-7 cell lines and VSMCs (Luciferase Report assay) method to study the ER alpha for Myocardin differentiation ability, the results showed that ER α can inhibit SM22 α Myocardin for transcription activation. At the same time, the expression of estradiol and tamoxifen treatment by transfection group for detection of SM22 and found that blocking the ER alpha for the inhibitory effect of Myocardin differentiation ability can be ER alpha antagonist tamoxi.