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Up-regulation of miR-26a promotes apoptosis of hypoxic rat neonatal cardiomyocytes by repressing GSK-3β protein expression.

Authors
 Jong Hui Suh  ;  Eunmi Choi  ;  Min-Ji Cha  ;  Byeong-Wook Song  ;  Onju Ham  ;  Se-Yeon Lee  ;  Cheesoon Yoon  ;  Chang-Yeon Lee  ;  Jun-Hee Park  ;  Sun Hee Lee  ;  Ki-Chul Hwang 
Citation
 BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.423(2) : 404-410, 2012 
Journal Title
 BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 
ISSN
 0006-291X 
Issue Date
2012
MeSH
Animals ; Apoptosis/genetics* ; Cell Hypoxia ; Cells, Cultured ; Gene Expression Regulation, Enzymologic* ; Glycogen Synthase Kinase 3/genetics* ; Glycogen Synthase Kinase 3 beta ; MicroRNAs/biosynthesis* ; MicroRNAs/genetics ; Myocytes, Cardiac/physiology* ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Up-Regulation
Keywords
MicroRNA-26a ; Cardiomyocytes ; Reactive oxygen species ; Apoptosis
Abstract
Myocardial ischemia is the major cause of morbidity and mortality due to cardiovascular diseases. This disease is a severe stress condition that causes extensive biochemical changes which trigger cardiac cell death. Stress conditions such as deprivation of glucose and oxygen activate the endoplasmic reticulum in the cytoplasm of cells, including cardiomyocytes, to generate and propagate apoptotic signals in response to these conditions. microRNAs (miRNAs) are a class of small non-coding RNAs that mediate posttranscriptional gene silencing. The miRNAs play important roles in regulating cardiac physiological and pathological events such as hypertrophy, apoptosis, and heart failure. However, the roles of miRNAs in reactive oxygen species (ROS)-mediated injury on cardiomyocytes are uncertain. In this study, we identified at the apoptotic concentration of H(2)O(2), miR-26a expression was increased. To determine the potential roles of miR-26a in H(2)O(2)-mediated cardiac apoptosis, miR-26a expression was regulated by a miR-26a or an anti-miR-26a. Overexpression of miR-26a increased apoptosis as determined by upregulation of Annexin V/PI positive cell population, caspase-3 activity and expression of pro-apoptotic signal molecules, whereas inhibition of miR-26a reduced apoptosis. We identified GSK3B as a direct downstream target of miR-26a. Furthermore, miR-26a attenuated viability and increased caspase-3 activity in normal cardiomyocytes. This study demonstrates that miR-26a promotes ROS-induced apoptosis in cardiomyocytes. Thus, miR-26a affects ROS-mediated gene regulation and cellular injury response.
Full Text
http://www.sciencedirect.com/science/article/pii/S0006291X12010376
DOI
22664106
Appears in Collections:
5. Research Institutes (연구소) > Yonsei Cardiovascular Research Institute (심혈관연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Park, Jun-Hee(박준희)
Song, Byeong Wook(송병욱)
Lee, Se Yeon(이세연)
Lee, Chang Yeon(이창연)
Cha, Min Ji(차민지)
Choi, Eun Mi(최은미)
Ham, On Ju(함온주)
Hwang, Ki Chul(황기철)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/89700
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