Fig. 3: Cardiac specific deletion of SNX16 alleviated AngII-induced cardiac hypertrophy via inhibiting the EGF/EGFR signaling pathway.
From: SNX16 aggravates AngII-induced cardiac hypertrophy in mice via EGFR transactivation
A, B The protein expression levels of SNX16, p-EGFR, p-ERK1/2 and BNP in the hearts of WT and SNX16CKO mice treated with or without AngII infusion were determined by western blot analysis (n = 3). These p-values are from unpaired t-tests and one way-ANOVA, *p < 0.05, **p < 0.01, ***p < 0.001. C, D Surface areas of H9c2 cells were determined by immunofluorescence analysis with phalloidin (red) and counterstained with DAPI (blue) with EGF (1 μg/mL, C) or AngII (200 nmol/L, D) stimulation for 24 h with or without pretreatment with AZD9291 (100 nmol/L). Scale bar: 50 μm. Quantitative surface area of H9c2 cells: μM2, cells ≥50. These p-values are from unpaired t-tests and one way-ANOVA, *p < 0.05, **p < 0.01, ***p < 0.001. The data are presented as the means ± SEMs, and three independent experiments were performed.
