miR-30 Regulates Mitochondrial Fission through Targeting p53 and the Dynamin-Related Protein-1 Pathway
Figure 8
miR-30 can influence mitochondrial fission and apoptosis in cardiac fibroblasts.
(A) Enforced expression of miR-30a or miR-30b is able to attenuate the expression levels of p53 and Drp1. Cardiomyocytes were infected with the adenoviral miR-30a or miR-30b at a moi of 100. Adenoviral β-galactosidase (β-gal) served as a control. 24 h after infection, cells were treated with 200 µM hydrogen peroxide. Immunoblot analysis of p53 and Drp1 were performed 6 h after treatment. (B,C) Enforced expression of miR-30a or miR-30b is able to inhibit mitochondrial fission and apoptosis induced by hydrogen peroxide. Cardiac fibroblasts were treated as described for (A). Mitochondrial fission (B) and apoptosis (C) were analyzed 6 h and 12 h after treatment, respectively. *p<0.05, compared with the hydrogen peroxide alone. Data are expressed as the mean±SEM of three independent experiments.