[Bax inhibitor 1 inhibits vascular calcification in mice by activating optic atrophy 1 expression].
Copyright policy )[Bax inhibitor 1 inhibits vascular calcification in mice by activating optic atrophy 1 expression].
To investigate the effects of Bax inhibitor 1 (BI- 1) and optic atrophy protein 1 (OPA1) on vascular calcification (VC).Mouse models of VC were established in ApoE-deficient (ApoE-/-) diabetic mice by high-fat diet feeding for 12 weeks followed by intraperitoneal injections with Nε-carboxymethyl-lysine for 16 weeks. ApoE-/- mice (control group), ApoE-/- diabetic mice (VC group), ApoE-/- diabetic mice with BI-1 overexpression (VC + BI-1TG group), and ApoE-/- diabetic mice with BI-1 overexpression and OPA1 knockout (VC+BI-1TG+OPA1-/- group) were obtained for examination of the degree of aortic calcification using von Kossa staining. The changes in calcium content in the aorta were analyzed using ELISA. The expressions of Runt-related transcription factor 2 (RUNX2) and bone morphogenetic protein 2 (BMP-2) were detected using immunohistochemistry, and the expression of cleaved caspase-3 was determined using Western blotting. Cultured mouse aortic smooth muscle cells were treated with 10 mmol/L β-glycerophosphate for 14 days to induce calcification, and the changes in BI-1 and OPA1 protein expressions were examined using Western blotting and cell apoptosis was detected using TUNEL staining.ApoE-/- mice with VC showed significantly decreased expressions of BI-1 and OPA1 proteins in the aorta (P=0.0044) with obviously increased calcium deposition and expressions of RUNX2, BMP-2 and cleaved caspase-3 (P= 0.0041). Overexpression of BI-1 significantly promoted OPA1 protein expression and reduced calcium deposition and expressions of RUNX2, BMP-2 and cleaved caspase-3 (P=0.0006). OPA1 knockdown significantly increased calcium deposition and expressions of RUNX2, BMP-2 and cleaved caspase-3 in the aorta (P=0.0007).BI-1 inhibits VC possibly by promoting the expression of OPA1, reducing calcium deposition and inhibiting osteogenic differentiation and apoptosis of the vascular smooth muscle cells.
- Chinese PLA General Hospital China (People's Republic of)
- Capital Medical University China (People's Republic of)
Mice, Knockout, Caspase 3, Myocytes, Smooth Muscle, Membrane Proteins, Core Binding Factor Alpha 1 Subunit, Muscle, Smooth, Vascular, Diabetes Mellitus, Experimental, GTP Phosphohydrolases, Mice, Apolipoproteins E, Osteogenesis, Optic Atrophy, Autosomal Dominant, Animals, Calcium, Vascular Calcification, Cells, Cultured, bcl-2-Associated X Protein
Mice, Knockout, Caspase 3, Myocytes, Smooth Muscle, Membrane Proteins, Core Binding Factor Alpha 1 Subunit, Muscle, Smooth, Vascular, Diabetes Mellitus, Experimental, GTP Phosphohydrolases, Mice, Apolipoproteins E, Osteogenesis, Optic Atrophy, Autosomal Dominant, Animals, Calcium, Vascular Calcification, Cells, Cultured, bcl-2-Associated X Protein
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