Myocardial ischemia/reperfusion (MI/R) injury induces myocardial damage and dysfunction. Increasing evidence has confirmed that circular RNAs (circRNAs) play crucial roles in regulating MI/R. Mmu-circ-0001380 has identified to be highly expressed in myocardium of MI/R mouse model. However, its biological function and molecular mechanism in MI/R injury are still unclear. Here, we demonstrated that knockdown of cric-0001380 attenuated myocardial injury of MI/R mice. In vitro, silence of circ-0001380 significantly enhanced viability, and inhibited apoptosis and oxidative stress in HL-1 cells under oxygen-glucose deprivation/reoxygenation (OGD/R). Mmu-miR-106b-5p interacted with circ-0001380, and suppressed the expression of pleckstrin homology domain and leucine rich repeat protein phosphatase 2 (Phlpp2). The miR-106b-5p/Phlpp2 axis mediated the effect of circ-0001380 on OGD/R-induced apoptosis through regulating the phosphorylation of p38, and further involved in regulating the viability and oxidative stress of HL-1 cells. In conclusion, circ-0001380 downregulation relieves MI/R injury via regulating the miR-106b-5p/Phlpp2 axis. The present study indicates that mmu-circ-0001380 exacerbates the myocardial ischemia/reperfusion injury through modulating the miR-106b-5p/Phlpp2 axis in vitro and in vivo.
Keywords: CircRNA; Myocardial ischemia/reperfusion injury; Oxidative stress; Oxygen–glucose deprivation/reoxygenation (OGD/R); ZFP644.
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.