ROS-mediated bidirectional regulation of miRNA results in distinct pathologic heart conditions
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| Titel: | ROS-mediated bidirectional regulation of miRNA results in distinct pathologic heart conditions |
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| Autoren: | Eunhyun Choi, Onju Ham, Seahyoung Lee, Hyang-Hee Seo, Chang Yeon Lee, Ina Yun, Min-Ji Cha, Se-Yeon Lee, Ki-Chul Hwang, Sun M. Han, Jun-Hee Park, Jiyun Lee, Soyeon Lim |
| Weitere Verfasser: | Seahyoung Lee, Soyeon Lim, Onju Ham, Se-Yeon Lee, Chang Yeon Lee, Jun-Hee Park, Jiyun Lee, Hyang-Hee Seo, Ina Yun, Sun M. Han, Min-Ji Cha, Eunhyun Choi, Ki-Chul Hwang, Park, Jun-Hee, Seo, Hyang Hee, Lee, Se Yeon, Lee, Chang Yeon, Lim, So Yeon, Ham, On Ju |
| Quelle: | Biochemical and Biophysical Research Communications. 465:349-355 |
| Verlagsinformationen: | Elsevier BV, 2015. |
| Publikationsjahr: | 2015 |
| Schlagwörter: | 0301 basic medicine, Cardiomegaly/metabolism, Cells, Apoptosis, Cardiomegaly, Reactive Oxygen Species/metabolism, Gene Expression Regulation/genetics, Trans-Activators/genetics, Heart Failure/genetics, Rats, Sprague-Dawley, 03 medical and health sciences, Animals, MicroRNAs/metabolism, Cells, Cultured, Heart Failure, 2. Zero hunger, 0303 health sciences, Cultured, Nuclear Proteins/metabolism, Myocardium, Nuclear Proteins, Heart, ROS, Cardiomegaly/genetics, Rats, Nuclear Proteins/genetics, MicroRNAs/genetics, MicroRNAs, Gene Expression Regulation, Trans-Activators, Myocardium/metabolism, Trans-Activators/metabolism, Sprague-Dawley, Heart Failure/metabolism, Reactive Oxygen Species, miRNA regulation |
| Beschreibung: | Under distinct pathological heart conditions, the expression of a single miRNA can display completely opposite patterns. However, the mechanism underlying the bidirectional regulation of a single miRNA and the clinical implications of this regulation remain largely unknown. To address this issue, we examined the regulation of miR-1, one of the most abundant miRNAs in the heart, during cardiac hypertrophy and ischemia/reperfusion (I/R). Our data indicated that different magnitudes and chronicities of ROS levels in cardiomyocytes resulted in differential expression of miR-1, subsequently altering the expression of myocardin. In animal models, the administration of a miR-1 mimic attenuated cardiac hypertrophy by suppressing the transverse aortic constriction-induced increase in myocardin expression, whereas the administration of anti-miR-1 ameliorated I/R-induced cardiac apoptosis and deterioration of heart function. Our findings indicated that a pathologic stimulus such as ROS can bidirectionally alter the expression of miRNA to contribute to the development of pathological conditions exhibiting distinct phenotypes and that the meticulous adjustment of the pathological miRNA levels is required to improve clinical outcomes. |
| Publikationsart: | Article |
| Dateibeschreibung: | 349~355 |
| Sprache: | English |
| ISSN: | 0006-291X |
| DOI: | 10.1016/j.bbrc.2015.07.160 |
| Zugangs-URL: | https://pubmed.ncbi.nlm.nih.gov/26253469 http://www.sciencedirect.com/science/article/pii/S0006291X15303892 http://europepmc.org/abstract/MED/26253469 https://ir.ymlib.yonsei.ac.kr/handle/22282913/141109 https://www.sciencedirect.com/science/article/pii/S0006291X15303892 https://pubmed.ncbi.nlm.nih.gov/26253469/ |
| Rights: | Elsevier TDM CC BY NC ND |
| Dokumentencode: | edsair.doi.dedup.....cf6da3f6423e40b32bae0795a116b177 |
| Datenbank: | OpenAIRE |
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Nájsť tento článok vo Web of Science | Abstract: | Under distinct pathological heart conditions, the expression of a single miRNA can display completely opposite patterns. However, the mechanism underlying the bidirectional regulation of a single miRNA and the clinical implications of this regulation remain largely unknown. To address this issue, we examined the regulation of miR-1, one of the most abundant miRNAs in the heart, during cardiac hypertrophy and ischemia/reperfusion (I/R). Our data indicated that different magnitudes and chronicities of ROS levels in cardiomyocytes resulted in differential expression of miR-1, subsequently altering the expression of myocardin. In animal models, the administration of a miR-1 mimic attenuated cardiac hypertrophy by suppressing the transverse aortic constriction-induced increase in myocardin expression, whereas the administration of anti-miR-1 ameliorated I/R-induced cardiac apoptosis and deterioration of heart function. Our findings indicated that a pathologic stimulus such as ROS can bidirectionally alter the expression of miRNA to contribute to the development of pathological conditions exhibiting distinct phenotypes and that the meticulous adjustment of the pathological miRNA levels is required to improve clinical outcomes. |
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| ISSN: | 0006291X |
| DOI: | 10.1016/j.bbrc.2015.07.160 |