[No authors listed]
In a previous study using a microRNA (miRNA/miR) microarray assay, we demonstrated that miR-133b-5p was upregulated in response to hypoxic preconditioning (HPC). The present study was designed to investigate the role of the miRâ133bâ5p in HPCâinduced cardioprotection and the underlying mechanisms involving caspaseâ8 and caspaseâ3 apoptotic signaling. Adult rats were subjected to myocardial ischemia/reperfusion (I/R) injury with or without ischemic preconditioning (IPC), and the level of miRâ133bâ5p in myocardium was measured. Neonatal rat cardiomyocytes were isolated and subjected to hypoxia/reoxygenation (H/R) injury, with or without HPC. miRâ133bâ5p antagomir was transfected into the cardiomyocytes to observe whether it could block HPCâinduced cardioprotection. Cellular injury was evaluated by detecting cell viability, lactate dehydrogenase (LDH) activity and apoptotic rate. Reverse transcriptionâquantitative polymerase chain reaction was used to measure the level of miRâ133bâ5p. The activation of caspaseâ8 and caspaseâ3 were measured by western blot analysis to detect the cleaved fragments as well as a colorimetric assay. Following myocardial I/R injury, the expression of miRâ133bâ5p was decreased in myocardium, while this decrease was restored by IPC. HPC protected neonatal rat cardiomyocytes against H/R injury by increasing cell viability, while reducing LDH release and cell apoptosis. These protective effects were coupled with the upregulation of miRâ133bâ5p. However, the knockdown of miRâ133bâ5p in the cardiomyocytes blocked HPCâmediated cardioprotection as reflected by the aggravation of cell injury and apoptosis. HPC upregulated miRâ133bâ5p level was markedly suppressed by the antagomir. In addition, the cleavage and activities of caspaseâ8 and caspaseâ3 were inhibited by HPC while reversed by knockdown of miRâ133bâ5p. Upregulation of miRâ133bâ5p contributes to HPCâmediated cardioprotection in cardiomyocytes, and the mechanism may be associated with inhibition of caspaseâ8 and caspaseâ3 apoptotic signaling.
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