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The long noncoding RNA XIST protects cardiomyocyte hypertrophy by targeting miR-330-3p

Chen, Yuewu, Liu, Xianxia, Chen, Lei, Chen, Weiwei, Zhang, Yuansheng, Chen, Jiaxian, Wu, Xuezheng, Zhao, Yong, Wu, Xiaoyan, Sun, Guowei
Biochemical and biophysical research communications 2018 v.505 no.3 pp. 807-815
binding sites, cardiomyocytes, cardiovascular diseases, hypertrophy, mice, microRNA, non-coding RNA, phenylephrine
Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are implicated in numerous kinds of cardiovascular diseases, and their vital role in regulating cardiac hypertrophy still needs to be explored. In this study, we demonstrated that lncRNA X-inactive specific transcript (XIST) was upregulated in hypertrophic cardiac of mice and phenylephrine (PE)-treated cardiomyocytes. Next, we observed that inhibition of XIST induced hypertrophic response of cardiomyocyte and overexpression of XIST attenuated cardiomyocyte hypertrophy induced by PE. Furthermore, through online predictive tools and functional experiments, we demonstrated that XIST and S100B were targets of miR-330-3p. XIST and miR-330-3p suppressed each other in a reciprocal way in cardiomyocytes. Additionally, XIST promoted S100B expression through harboring the complementary binding sites with miR-330-3p, eventually prevented cardiac hypertrophy. In conclusion, our findings revealed a novel molecular mechanism that XIST/miR-330-3p/S100B pathway modulates the progression of cardiomyocyte hypertrophy.