Fig. 6

P300 and P53 competitively bind HIF-1α to regulate HMOX1 expression during ferroptosis of HASMCs. A-B. Western blot analysis and quantification results showing SLC7A11, GPX4, and FSP1 protein levels after CD (A), and IKE (B) stimulation in HASMCs infected with lenti-shRNA, lenti-shP300-1 and lenti-shP300-2 (A-B), β-actin served as a loading control (n = 4 per group). C-D. Western blot analysis and quantification results showing HMOX1 protein levels in HASMCs infected with lenti-shRNA, lenti-shP300-1 and lenti-shP300-2 after CD and IKE stimulation. β-actin served as a loading control (n = 4 per group). E. Co-immunoprecipitation results showed that endogenous P300 interacted with exogeneous HIF-1α in HASMCs after treatment with MG132. F. The interaction between endogenous HIF-1α and exogenous P300 in 293T cells after treatment with MG132 was verified by Co-immunoprecipitation. G. Co-immunoprecipitation showed the interaction between endogenous HIF-1α and endogenous P300 and P53 after treatment with CD and MG132 in nucleus of HASMCs. Values are means ± SD; ***p < 0.001, NS, no significant