Fig. 5
From: SBK3 suppresses angiotensin II-induced cardiac hypertrophy by regulating mitochondrial metabolism
The mitochondrial protein SBK3 rebalanced the level of oxidative stress and energy metabolism in cardiomyocytes induced by Ang II. (A) SBK3 was located in the mitochondria of rat cardiomyocytes, evidenced by Western blot, similar data in three experiment. (B, C) Verification of SBK3 overexpression in ARCMs based on (B, scale bar = 100 μm) GFP fluorescence and (C) protein (western blot) expression (D) Representative images of SBK 3 expression (anti-SBK3 or anti-Flag) co-localized with mitochondria, scale bar = 25 μm. (E) Overexpression of SBK3 restored the level of mitochondrial ROS induced by Ang II in ARCMs stained with DCFH-DA, as shown by confocal microscopy, scale bar = 10 μm. (F–H) Overexpression of SBK3 reduced the levels of MDA (F, n = 6), increased the level of SOD in mitochondria (SOD2) (H, n = 4) but not in the cytoplasm (total SOD) (G, n = 6). (I,J) Overexpression of SBK3 enhanced the production of ATP (I, n = 5) and the rate of oxygen consumption (J, n = 4) in the ARCMs induced by Ang II (5 μM, 24 h). The data were expressed as Mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, ns, non significant; one-way ANOVA test, followed by the Newman–Keuls test.
