Skip to main content
Fig. 5 | Cellular & Molecular Biology Letters

Fig. 5

From: G6PD maintains the VSMC synthetic phenotype and accelerates vascular neointimal hyperplasia by inhibiting the VDAC1–Bax-mediated mitochondrial apoptosis pathway

Fig. 5

The antiapoptotic effects of G6PD on PDGF-BB-induced VSMC proliferation and viability are mediated by VDAC1. The expression of VDAC1 was reduced by siRNA in VSMCs, and G6PD was subsequently overexpressed by an adenovirus encoding an HA tag. Finally, the cells were treated with PDGF-BB for 12 h. A, B TUNEL analysis was used to analyze cell apoptosis, and the TUNEL-positive cell ratio was quantified from 5 microscopic views in each experiment. n = 5. Scale bar = 100 µm. C The viability of VSMCs was assessed by a CCK8 assay. n = 5. D Cell proliferation was measured by a cell counting experiment. n = 6. Ad-Null and si-Con were used as negative controls. E G6PD-NTD virus infection inhibited VSMC apoptosis, and western blotting was performed three times; representative images are presented. F G6PD-NTD virus infection promoted VSMC survival. Statistical significance was determined using two-way ANOVA in BD, F. *P < 0.05; **P < 0.01; ***P < 0.001; ns, no significant difference

Back to article page