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Mol Cells ; 40(12): 916-924, 2017 Dec 31.
Artigo em Inglês | MEDLINE | ID: mdl-29237256

RESUMO

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 Gadd45ß (growth arrest DNA damage-inducible gene 45ß) 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 Gadd45ß. In summary, this study demonstrates that miR-206 could protect against myocardial I/R injury by targeting Gadd45ß.


Assuntos
Antígenos de Diferenciação/genética , MicroRNAs/genética , Traumatismo por Reperfusão Miocárdica/prevenção & controle , Animais , Antígenos de Diferenciação/metabolismo , Modelos Animais de Doenças , Masculino , MicroRNAs/metabolismo , Traumatismo por Reperfusão Miocárdica/genética , Ratos , Ratos Sprague-Dawley
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