Long Non-Coding RNA-ROR Mediates the Reprogramming in Cardiac Hypertrophy

被引:97
作者
Jiang, Feng [1 ]
Zhou, Xiangyu [2 ]
Huang, Jing [1 ]
机构
[1] Chongqing Med Univ, Affiliated Hosp 2, Dept Cardiol, Chongqing, Peoples R China
[2] Southwest Med Univ, Affiliated Hosp, Dept Vasc & Thyroid Surg, Luzhou, Sichuan, Peoples R China
关键词
CARDIOMYOCYTE HYPERTROPHY; HEART-FAILURE; MICRORNAS; TRANSCRIPTION; ROLES; CELLS;
D O I
10.1371/journal.pone.0152767
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Background Cardiac hypertrophy associated with various cardiovascular diseases results in heart failure and sudden death. A clear understanding of the mechanisms of hypertrophy will benefit the development of novel therapies. Long non-coding RNAs (lncRNAs) have been shown to play essential roles in many biological process, however, whether lncRNA-ROR plays functional roles in the reprogramming of cardiomyocyte remains unclear. Methodology/Principal Findings Here we show that lncRNA-ROR plays important roles in the pathogenesis of cardiac hypertrophy. In hypertrophic heart and cardiomyocytes, the expression of lncRNA-ROR is dramatically increased, downregulation of which attenuates the hypertrophic responses. Furthermore, the expression of lncRNA-ROR negatively correlates with miR-133, whose expression is increased when lncRNA-ROR is knocked down. In line with this, overexpression of miR-133 prevents the elevation of lncRNA-ROR and re-expression of ANP and BNP in cardiomyocytes subject to phenylephrine treatment. Conclusions/Significance Taken together, our study demonstrates that lncRNA-ROR promotes cardiac hypertrophy via interacting with miR-133, indicating that lncRNA-ROR could be targeted for developing novel antihypertrophic therapeutics.
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页数:10
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