Increased Dp71 in ischemia-reperfusion injured rat heart exerts anti-apoptotic role via enhancing Bcl-2

For the first time, increased Dp71 in ischemia-reperfusion injured rat heart were identified, both Dp71 mRNA and protein reached its peak expression 8 h after reperfusion. In H2O2 stimulated H9c2 cells, Dp71 mRNA and protein gradually increased and reached a peak at 16 h. Enhanced Dp71 in H9c2 could resist H2O2-induced cell apoptosis, while Dp71 depletion accelerated the apoptosis induced by H2O2. Enhanced Bcl-2 expression and Bcl-2/Bax protein expression ratio was identified in Dp71 overexpressed H9c2 cells, while knocking down Dp71 significantly decreased the Bcl-2 and Bcl-2/Bax protein expression ratio. Increased Dp71 can accelerate FAK and p65 phosphorylation, which finally resulted in enhanced Bcl-2 expression and explains the highly possible cardiac protection role of Dp71.

Automated summary

This study identified the increased expression of Dp71 in ischemia-reperfusion injured rat hearts and its protective role against H2O2-induced apoptosis in H9c2 cells. The upregulation of Bcl-2 expression and FAK and p65 phosphorylation may contribute to the cardiac protective effects of Dp71.