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• W2908528740 abstract "Myocardial ischemia-reperfusion (I/R) is a common and lethal disease that threatens people’s life worldwide. The underlying mechanisms are under intensive study and yet remain unclear. Here, we explored the function of miR-322/503 in myocardial I/R injury. We used isolated rat perfused heart as an in vivo model and H9c2 cells subjected with the oxygen and glucose deprivation followed by reperfusion as in vitro model to study myocardial I/R injury. 2,3,5-Triphenyltetrazolium chloride (TTC) staining was used to measure the infarct size, and terminal deoxynucleotidyl transferase dUTP-mediated nick-end label (TUNEL) staining was used to examine apoptosis. Quantitative RT-PCR and Western blot were used to determine expression levels of miR-322/503, Smad ubiquitin regulatory factor 2 (Smurf2), enhancer of zeste homolog 2 (EZH2), p-Akt, and p-GSK3β. Overexpression of miR-322/503 decreased infarct size, inhibited cell apoptosis, and promoted cell proliferation through upregualtion of p-Akt and p-GSK3β. Thus the expression of miR-322/503 was reduced during I/R process. On the molecular level, miR-322/503 directly bound Smurf2 mRNA and suppressed its translation. Smurf2 ubiquitinated EZH2 and degraded EZH2, which could activate Akt/GSK3β signaling. Our study demonstrates that miR-322/503 plays a beneficial role in myocardial I/R injury. By inhibition of Smurf2 translation, miR-322/503 induces EZH2 expression and activates Akt/GSK3β pathway, thereby protecting cells from ischemia reperfusion injury." @default.
• W2908528740 created "2019-01-25" @default.
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• W2908528740 date "2019-08-01" @default.
• W2908528740 modified "2023-10-14" @default.
• W2908528740 title "Inhibition of Smurf2 translation by miR-322/503 protects from ischemia-reperfusion injury by modulating EZH2/Akt/GSK3β signaling" @default.
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• W2908528740 doi "https://doi.org/10.1152/ajpcell.00375.2018" @default.
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