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MicroRNA-206 Protects against Myocardial Ischaemia-Reperfusion Injury in Rats by Targeting Gadd45β

  • Zhai, Changlin (Department of Cardiovascular Diseases, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University) ;
  • Qian, Qang (Department of Cardiovascular Diseases, The Frist Affiliated Hospital of Jiaxing University) ;
  • Tang, Guanmin (Department of Cardiovascular Diseases, The Frist Affiliated Hospital of Jiaxing University) ;
  • Han, Bingjiang (Department of Cardiovascular Diseases, The Frist Affiliated Hospital of Jiaxing University) ;
  • Hu, Huilin (Department of Cardiovascular Diseases, The Frist Affiliated Hospital of Jiaxing University) ;
  • Yin, Dong (Department of Cardiovascular Diseases, The Frist Affiliated Hospital of Jiaxing University) ;
  • Pan, Haihua (Department of Cardiovascular Diseases, The Frist Affiliated Hospital of Jiaxing University) ;
  • Zhang, Song (Department of Cardiovascular Diseases, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University)
  • Received : 2017.08.15
  • Accepted : 2017.10.26
  • Published : 2017.12.31

Abstract

MicroRNAs are widely involved in the pathogenesis of cardiovascular diseases through regulating gene expression via translational inhibition or degradation of their target mRNAs. Recent studies have indicated a critical role of microRNA-206 in myocardial ischaemia-reperfusion (I/R) injury. However, the function of miR-206 in myocardial I/R injury is currently unclear. The present study was aimed to identify the specific role of miR-206 in myocardial I/R injury and explore the underlying molecular mechanism. Our results revealed that the expression level of miR-206 was significantly decreased both in rat I/R group and H9c2 cells subjected to hypoxia/reoxygenation (H/R) compared with the corresponding control. Overexpression of miR-206 observably decreased infarct size and inhibited the cardiomyocyte apoptosis induced by I/R injury. Furthermore, bioinformatics analysis, luciferase activity and western blot assay proved that $Gadd45{\beta}$ (growth arrest DNA damage-inducible gene $45{\beta}$) was a direct target gene of miR-206. In addition, the expression of pro-apoptotic-related genes, such as p53, Bax and cleaved caspase3, was decreased in association with the down-regulation of $Gadd45{\beta}$. In summary, this study demonstrates that miR-206 could protect against myocardial I/R injury by targeting $Gadd45{\beta}$.

Keywords

References

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