Fig. 6: VNS improved cardiomyocytes metabolic process in infracted heart through VEGF signaling. | Cell Death & Disease

Fig. 6: VNS improved cardiomyocytes metabolic process in infracted heart through VEGF signaling.

From: Vagus nerve stimulation optimized cardiomyocyte phenotype, sarcomere organization and energy metabolism in infarcted heart through FoxO3A-VEGF signaling

Fig. 6

A and B Typical image of CPT1α and GLUT4 in VNS-MI hearts with or without the treatment of knockdown of VEGF-A or VEGF-B by shRNA, or VEGFR1 blocker AMG as determined by immunohistochemically staining. C–F VNS increased CPT1α and GLUT4 in infraction area of the infarcted heart as evaluated by western blot, and knockdown of VEGF-A or VEGF-B by shRNA, or VEGFR1 blocker AMG markedly abolished the effect of VNS on CPT1α and GLUT4 expressions in infraction area of the infarcted hearts. knockdowning VEGF-A more obviously reduced GlUT4 expression in the infarcted heart compared to that by knockdowning VEGF-B. By contrast, knockdowning VEGF-B more obviously reduced CPT1ɑ expression in the infarcted heart compared to that by knockdowning VEGF-A and VEGFR1 blocker AMG reversed VNS-mediated both CPT1α and GLUT4 changes compared with that by knockdowning VEGF-A or VEGF-B. AMG effectively abolished the inhibition role of VNS in reducing PDK4 expression. However, knockdown of VEGF-A or VEGF-B by shRNA not only did not reverse, but also enhanced the inhibitory effects of VNS on PDK4. n = 3, *P < 0.05 vs. MI; #P < 0.05 vs. MI; @P < 0.05 vs. VNS; &P < 0.05 vs. VNS; $P < 0.05 vs. VNS. For all scatter plots, data are mean ± SEM; one-way ANOVA with Bonferroni post hoc testing.

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