Fig. 7: FoxO3A involved in alteration of VNS-mediated cardiomyocytes phenotype, sarcomere organization, and energy metabolism.
A and B VNS increased the levels of pFoxO3A in the infarcted heart as evaluated by western blot A. B Semi-quantitative analysis of pFoxO3A as indicated. n = 3,*P < 0.05 vs. Sham; &P < 0.05 vs. MI. C Typical image of decreased nuclear translocation by VNS in the infarcted heart. D ACh-induced expression of α-MHC, β-MHC, CPT1α, CPT1β, and GLUT4, the specific effects could be substantially abolished by over-expressing FoxO3A as determined by western blot. E ACh improved sarcomere organization in H9c2 myoblasts cells disturbed by NE under differentiation medium (DM), and the effective role could be obviously abrogated by over-expressing FoxO3A as determined by α-Actinin staining. F ACh reversed the enhanced effects of NE on sarcomere F-actin assembly in myocytes through FoxO3A. Typical image for F-Actin in H9c2 cells transfected with Ad-shFoxO3A (MOI:100) under proliferation medium (PM) with continuous 10−5 Mol/L NE and/or 10−8 Mol/L ACh as determined by F-Actin staining. G Oxygen consumption rates (OCR) at baseline and in the presence of oligomycin, FCCP [carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone], and antimycin A + rotenone (AA + R). n = 3 independent experiments. *P < 0.05 vs. DM + NE. #P < 0.05 vs. DM + NE. H ACh improved glucose uptake in H9c2 myoblasts cells inhibited by NE, and the effective role could be obviously canceled by over-expressing FoxO3A. I ACh increased ATP production in H9c2 myoblasts cells reduced by NE, which could be obviously reversed by over-expressing FoxO3A. n = 3, *P < 0.05 vs. DM; &P < 0.05 vs. DM and NE; #P < 0.05 vs. NE; $P < 0.05 vs. ACh; @P < 0.05 vs. NE + ACh. For all scatter plots, data are mean ± SEM; one-way ANOVA with Bonferroni post hoc testing.
