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

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 biolog...

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Bibliographic Details
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
Online Access:Get full text
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Summary: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.
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Competing Interests: The authors have declared that no competing interests exist.
Conceived and designed the experiments: XZ JH. Performed the experiments: FJ XZ. Analyzed the data: FJ XZ. Contributed reagents/materials/analysis tools: FJ XZ. Wrote the paper: FJ JH.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0152767