Albumin nanoparticles equipped with miR-24 agonist mediate transforming growth factor (TGF)-β signaling pathway to inhibit hypoxia-induced myocardial cell apoptosis

Abstract

Abnormal expression of miR-24 is related to cardiomyocyte apoptosis. This study mainly explored the role of miR-24 in cardiomyocyte apoptosis and its possible mechanism. Cardiomyocytes were obtained from newborn SD mice and were randomly separated into blank group, hypoxia group (hypoxia), miR-24 group (hypoxia+miR-24 agonist nano albumin particles), and pathway agonist (hypoxia+miR-24 agonist nano albumin particles+TGF-β signaling pathway inhibitor) group. miR-24 level in hypoxia group and pathway agonist group was sharply decreased when compared to that of the blank or miR-24 group (P < 0.05). Cell survival rate and apoptosis of hypoxia group and pathway agonist were also significantly inhibited when compared to that of blank or miR-24 group (P < 0.05). The expression levels of TGF-β, Smad, p-Smad, caspsase-3, Bcl-2, and HIF-1a were sharply up-regulated in hypoxia group and pathway agonists group, compared to blank group and miR-24 group (P < 0.05). miR-24 can inhibit cardiomyocyte apoptosis through interaction with TGF-β signaling pathway factors, to up-regulate the TGF-β pathway factor expression and activate TGF-β signaling. TGF-β also interacts with downstream factor Smad to activate the Smad pathway and phosphorylate Smad, thereby activating the activity of HIF-1a, up-regulating HIF-1a, and inhibiting the expression of apoptotic proteins caspsase-3 and Bcl-2.