Fig. 3 | Signal Transduction and Targeted Therapy

Fig. 3

From: Arginase 1 drives mitochondrial cristae remodeling and PANoptosis in ischemia/hypoxia-induced vascular dysfunction

Fig. 3

Exposure of VSMCs to hypoxia enhances the interaction between Arg1 and Mic10, eliciting conformational alterations in Mic10. a A schema illustrates the LC-MS/MS approach for detecting Arg1-interacting proteins. b A Venn diagram identified proteins that bind to Arg1. c A schematic representation of the mitochondrial cristae structure and the MICOS complex. OMM outer mitochondrial membrane, IMM inner mitochondrial membrane. d Molecular docking between Arg1 and Mic10, and the visualization of the binding sites are presented. e A co-immunoprecipitation (Co-IP) assay confirmed the interaction between Arg1 and Mic10 (n = 3 independent experiments). f Co-IP experiment assessed the impact of siArg1 on the interaction of Arg1 and Mic10 (n = 3 independent experiments). g Immunofluorescence microscopy revealed the colocalization of Arg1 and Mic10, shown in green and red, respectively, scale bars correspond to 8 μm for low-magnification images and 4 μm for high-magnification views (n = 3 independent experiments). h, i The expression and statistical analysis of Arg1 in total, cytoplasmic, and mitochondrial fractions of VSMCs following hypoxia. β-actin, Tubulin, and COX IV served as internal references for the total, cytoplasmic, and mitochondrial fractions, respectively (n = 3 independent experiments). j, k The expression and statistical analysis of Arg1 in total, cytoplasmic, and mitochondrial fractions of hypoxic VSMCs after being treated with siRNA (n = 3 independent experiments). l Arg1 binds to Mic10 and inhibits the polymerization between MIC10 monomers. m The Root Mean Square Deviation analysis. n The radius of gyration (Rg) analysis. o Analysis of hydrogen bond formation. a: p < 0.05, as compared with the Normal group; b: p < 0.05, as compared with the Hypoxia + siNC group

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