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


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 $Gadd45{\beta}$.


Supported by : Zhejiang province medical and health science and technology Research fund, Zhejiang Province Traditional Chinese Medicine Scientific Research Fund, Jiaxing cardiovascular key discipline fund, Zhejiang Province chronic diseases Base fund, Jiaxing key innovation team fund


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