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논문 기본 정보

자료유형
학술저널
저자정보
Changlin Zhai (Shanghai Jiao Tong University) Qang Qian (The Frist Affiliated Hospital of Jiaxing University) Guanmin Tang (The Frist Affiliated Hospital of Jiaxing University) Bingjiang Han (The Frist Affiliated Hospital of Jiaxing University) Huilin Hu (The Frist Affiliated Hospital of Jiaxing University) Dong Yin (The Frist Affiliated Hospital of Jiaxing University) Haihua Pan (The Frist Affiliated Hospital of Jiaxing University) Song Zhang (Shanghai Jiao Tong University)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells 제40권 제12호
발행연도
2017.12
수록면
916 - 924 (9page)

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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 un-clear. 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 expres-sion 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 Gadd45beta (growth arrest DNA damage-inducible gene 45beta) 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 Gadd45beta. In summary, this study demonstrates that miR-206 could protect against myocardial I/R injury by targeting Gadd45beta.

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