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Isolation and Characterization of Primary Rat Valve Interstitial Cells: A New Model to Study Aortic Valve Calcification
Published on: November 20, 2017
Knockdown of PARM1 Alleviates Aortic Valve Calcification via the PRKCH-MAPK Signaling Pathway
Haochang Hu1, Xian Zhu2, Jinyong Chen1
1Department of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China; State Key Laboratory of Transvascular Implantation Devices, Hangzhou, Zhejiang, China; Heart Regeneration and Repair Key Laboratory of Zhejiang Province, Hangzhou, Zhejiang, China.
None:
With the aging of the population, the prevalence of calcific aortic valve disease (CAVD) has increased yearly. However, effective means to delay or even reverse the progression of CAVD are still lacking. This study revealed that prostate androgen-regulated mucin-like protein 1 (PARM1) expression was significantly up-regulated in calcified aortic valve tissues. Functional investigations demonstrated that PARM1 knockdown effectively suppressed osteogenic differentiation of valvular interstitial cells (VICs) and mitigated pathological aortic valve calcification. Mechanically, PARM1 knockdown down-regulated PRKCH mRNA expression, consequently attenuating MAPK pathway activation during the osteogenic differentiation of VICs. In conclusion, PARM1 could be a feasible target for CAVD prevention.
