Fig. 2: Cardiac specific deletion of SNX16 reduced AngII-induced cardiac hypertrophy in mice.

A A schematic diagram of generating heart-specific SNX16 knockout mice. B Representative PCR genotyping was determined by PCR with mouse tail genomic DNA. A 400 bp fragment for wild type C57Bl/6, a 458 bp fragment for SNX16^Fl/Fl, and a 400 bp fragment for Cre were amplified by PCR. C Expression of Snx16 mRNA in the hearts of WT (f/f-) and SNX16^CKO (f/f Cre+) mice was determined by RT‒PCR; n = 4‒5. The p-value is from unpaired t-tests, **p < 0.01. D, E Expression of SNX16 protein in the hearts of WT and SNX16^CKO mice was detected by western blot analysis (n = 3). The p-values is from unpaired t-tests, *p < 0.05. F Images of hearts from WT and SNX16^CKO mice with or without AngII infusion. Scale bar: 5 mm. G, H Ratios of HW/BW and LW/BW were obtained for WT and SNX16^CKO mice, n = 6. These p-values are from unpaired t-tests and one way-ANOVA, *p < 0.05, ***p < 0.001. I Heart tissues with transverse sections were analyzed by H&E staining. Scale bar: 1 mm. n = 3. J, K Representative images and summary data were analyzed with wheat germ agglutinin (WGA) staining. Scale bar: 50 μm. Mice, n = 3; cells ≥50 from three independent experiments. These p-values are from unpaired t-tests and one way-ANOVA, *p < 0.05. The data are presented as the means ± SEMs.