Abstract: Objective To investigate the expression of c-Ski and its role in p38 regulation in the endothelial-to-mesenchymal transition ( EndMT) in human coronary artery endothelial cells, which may provide novel targets for prevention and treatment of myocardial fibrosis. Methods The EndMT model was constructed in HCAECs using TGF-β1. The expression of c-Ski and EndMT markers was detected by quantitative real-time PCR and Western blotting. Results c-Ski was down-regulated after TGF-β1 treatment in the HCAECs. Overexpression of c-Ski suppressed TGF-β1-induced EndMT in HCAECs. The overexpression of c-Ski down-regulated the expression of α-SMA and vimentin, and up-regulated the expression of CD31 in TGF-β1-induced HCAECs ( P < 0. 01 ). The treatment with p38 inhibitor SB203580 further promoted TGF-β1-induced-EndMT in HCAECs; p38 signaling was activated after overexpression of c-Ski. Use of p38 inhibitor SB203580 could partially rescue the inhibitory effect of c-Ski overexpression on TGF-β1-induced EndMT in HCAECs. Conclusion c-Ski suppressed the TGF-β1-induced EndMT of HCAECs via regulating p38 activation. 

Key words: c-Ski, endothelial to mesenchymal transition, p38 signaling pathway, human coronary artery endothelial cells