Fig. 3: COMP−/− VSMCs exhibit mitochondrial oxidative phosphorylation dysfunction. | Cell Death & Disease

Fig. 3: COMP−/− VSMCs exhibit mitochondrial oxidative phosphorylation dysfunction.

From: COMP-prohibitin 2 interaction maintains mitochondrial homeostasis and controls smooth muscle cell identity

Fig. 3Fig. 3

a Microarray analysis of the KEGG pathway downregulated by COMP deficiency. b Heatmap of representative genes involved in oxidative phosphorylation. c RT-qPCR validation of the genes related to oxidative phosphorylation downregulated by COMP deficiency in VSMCs. The data was analyzed using unpaired two-tailed Student’s t test and presented as the means ± SD of three independent experiments. *P < 0.05. d Traces of mitochondrial oxygen consumption rates of rat VSMCs measured using the Seahorse XF24 flux analyzer, with sequential injections of mitochondrial effectors at time points indicated by the downward arrows. The data were analyzed using unpaired two-tailed Student’s t test and presented as the means ± SD of four independent experiments. *P < 0.05. e Intracellular ATP production of rat VSMCs. The data were analyzed using unpaired two-tailed Student’s t test and presented as the means ± SD of four independent experiments. *P < 0.05. f Intracellular ATP production of scrambled siRNA-transfected and COMP siRNA-transfected VSMCs transplanted with scrambled or COMP siRNA-transfected mitochondria. The data were analyzed using one-way ANOVA followed by the Student–Newman–Keuls test for post-hoc comparison and presented as the means ± SD of four independent experiments in duplicate. *P < 0.05. g Traces and quantification of the mitochondrial oxygen consumption rates of scrambled siRNA-transfected VSMCs transplanted with scrambled or COMP siRNA-transfected mitochondria. The data were analyzed using unpaired two-tailed Student’s t test and presented as the means ± SD of six independent experiments. *P < 0.05

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