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The present work addressed the hypothesis that NG2/ CSPG4 , CD146/ MCAM , and VAP1/ AOC3  are target genes of myocardin-related transcription factors (MRTFs: myocardin/ MYOCD , MRTF-A/ MKL1 , MRTF-B/ MKL2 ) and serum response factor ( SRF ). Using a bioinformatics approach, we found that  CSPG4 ,  MCAM , and  AOC3  correlate with  MYOCD , MRTF-A/ MKL1 , and  SRF  across human tissues. No other transcription factor correlated as strongly with these transcripts as  SRF . Overexpression of MRTFs increased both mRNA and protein levels of  CSPG4 ,  MCAM , and  AOC3  in cultured human smooth muscle cells (SMCs). Imaging confirmed increased staining for CSPG4, MCAM, and AOC3 in MRTF-A/ MKL1 -transduced cells. MRTFs exert their effects through SRF, and the  MCAM  and  AOC3  gene loci contained binding sites for SRF. SRF silencing reduced the transcript levels of these genes, and time-courses of induction paralleled the direct target  ACTA2 . MRTF-A/ MKL1  increased the activity of promoter reporters for  MCAM  and  AOC3 , and transcriptional activation further depended on the chromatin remodeling enzyme KDM3A.  CSPG4 ,  MCAM , and  AOC3  responded to the MRTF-SRF inhibitor CCG-1423, to actin dynamics, and to ternary complex factors. Coincidental detection of these proteins should reflect MRTF-SRF activity, and beyond SMCs, we observed co-expression of CD146/ MCAM , NG2/ CSPG4 , and VAP1/ AOC3  in pericytes and endothelial cells in the human brain. This work identifies highly responsive vascular target genes of MRTF-SRF signaling that are regulated via a mechanism involving KDM3A.

NG2/CSPG4, CD146/MCAM and VAP1/AOC3 are regulated by myocardin-related transcription factors in smooth muscle cells