Figure 5.

MiR-532-3p can regulate mitochondrial fission and apoptosis in cardiomyocytes treated by DOX. (a and b) Mitochondrial fission (a) and cell death (b) were not changed in neonatal rat cardiomyocytes overexpressing miR-532-3p for the indicated times. (c and d) Enfored expression of miR-532-3p enhanced mitochondrial fission (c) and cell death (d) in cardiomyocytes upon DOX (0.2 μM) treatment. Representative photos showed mitochondrial fission (c, left). Blue, DAPI (4,6-diamidino-2-phenylindole)-stained nuclei; red, MitoTracker Red CMXRos-stained mitochondria. Scale bar, 10μM. The percentage of cells undergoing mitochondrial fission were counted (c, right). (e and f) Inhibition of endogenous miR-532-3p using miR-532-3p antagomir prevented mitochondrial fission (e) and cell death (f) in cardiomyocytes treated with DOX (2 μM). Data are expressed as the mean±S.D., n=3. *P<0.05