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

• Published in: PloS one Vol. 11; no. 4; p. e0152767
• Main Authors: Jiang, Feng, Zhou, Xiangyu, Huang, Jing
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 15.04.2016; Public Library of Science (PLoS)
• Subjects: Animals; Biological activity; Biology and Life Sciences; Cardiology; Cardiomegaly - genetics; Cardiomegaly - pathology; Cardiomyocytes; Cardiovascular diseases; Coronary artery disease; Coronary vessels; Deoxyribonucleic acid; DNA; DNA damage; Gene expression; Gene Expression Regulation - drug effects; Gene Knockdown Techniques; Genetic aspects; Heart diseases; Heart failure; Heart hypertrophy; Hospitals; Hypertrophy; Kinases; Laboratory animals; Male; Medicine and Health Sciences; Mice; Mice, Inbred C57BL; MicroRNA; MicroRNAs; MicroRNAs - genetics; Myocytes, Cardiac - drug effects; Myocytes, Cardiac - pathology; Non-coding RNA; Pathogenesis; Phenylephrine; Phenylephrine - pharmacology; Physiological aspects; Plasmids; Research and Analysis Methods; Ribonucleic acid; Risk factors; RNA; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; Stem cells; Ventilators; China
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0152767

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. 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. 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.