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Fig. 6 | Cellular & Molecular Biology Letters

Fig. 6

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

Fig. 6

G6PD competes with Bax for binding VDAC1 by reducing its oligomerization. A, B Coimmunoprecipitation (IP) assays were used to detect the interaction between VDAC1-Bax (A) and VDAC1-Bcl-2 (B) in VSMCs stimulated with or without PDGF-BB for 12 h, respectively. C, D The interaction between VDAC1 and Bax in VSMCs was examined by IP after the administration of 6-AN (C) or siG6PD (D). E, F After the addition of 6-AN (E) or siG6PD (F), G6PD was overexpressed, and the interaction between VDAC1 and Bax in VSMCs was examined by IP. G–I Oligomerization of VDAC1 was detected by WB analysis with or without PDGF-BB stimulation for 12 h (G). After treatment with siG6PD (H) or 6AN (I), G6PD-overexpressing cells were used for further study

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Cellular & Molecular Biology Letters

ISSN: 1689-1392

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