Data from: Inhibition of Smurf2 translation by miR-322/503 protects from ischemia reperfusion injury by modulating EZH2/Akt/GSK3β signaling

BACKGROUND: 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. METHODS: We
used isolated rat perfused heart as an in vivo model and H9c2 cells
subjected with the oxygen and glucose deprivation followed by reperfusion
(OGD/R) as in vitro model to study myocardial I/R injury. TTC staining was
used to measure the infarct size and TUNEL staining was used to examine
apoptosis. qRT-PCR and western blot were used to determine expression
levels of miR-322/503, Smurf2, EZH2, p-Akt, p-GSK3β. RESULTS:
Overexpression of miR-322/503 decreased infarct size, inhibited cell
apoptosis and promoted cell proliferation through up-regulation 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. CONCLUSIONS: 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.