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

被引:44
作者
Chen, Yuewu [1 ]
Liu, Xianxia [1 ]
Chen, Lei [1 ]
Chen, Weiwei [1 ]
Zhang, Yuansheng [1 ]
Chen, Jiaxian [1 ]
Wu, Xuezheng [1 ]
Zhao, Yong [1 ]
Wu, Xiaoyan [1 ]
Sun, Guowei [1 ]
机构
[1] Hainan Med Univ, Affiliated Hosp 2, Dept Cardiovasc Med, 48 Baishuitang Rd, Haikou 570100, Hainan, Peoples R China
关键词
Cardiac hypertrophy; Cardiomyocyte; Long noncoding RNA; XIST; miR-330-3p; S100B; CARDIAC-HYPERTROPHY; CANCER PROLIFERATION; CELL-PROLIFERATION; EXPRESSION; MECHANISMS; MICRORNAS; PROGNOSIS; APOPTOSIS; ONCOGENE; S100B;
D O I
10.1016/j.bbrc.2018.09.135
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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. (C) 2018 Elsevier Inc. All rights reserved.
引用
收藏
页码:807 / 815
页数:9
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