Fig. 1: p22phox is upregulated in the failing human heart and in cardiomyocytes in response to pressure overload.
From: p22phox prevents the oxidation of SERCA2a and stabilizes it in the heart
a,b, Human heart LV samples obtained from healthy donor hearts and from patients with DCM or ICM were analyzed for p22phox protein expression levels (n = 8). a, The protein levels of p22phox, analyzed by western blotting with GAPDH as a loading control, in normal, DCM and ICM human heart LV lysates. b, Relative p22phox protein levels. c–e, Mice were subjected to TAC (1 week (1W) or 4 weeks (4W)) or sham operation, and the pressure gradient was assessed by Doppler on day 2 to confirm that appropriate levels of constriction were applied. After TAC, the heart LV tissues were analyzed for mRNA and protein expression. c, Relative p22phox mRNA levels (Sham and TAC 1W n = 7 and TAC 4W n = 8). d, The protein levels of p22phox were analyzed from whole heart tissue by western blotting with tubulin as loading control. e, The relative p22phox protein levels (n = 6). f–h, Following TAC 1W or sham operation, cardiomyocytes were isolated from adult mouse heart LV tissue and analyzed for protein and mRNA expression. f, The p22phox mRNA levels (Sham n = 8 and TAC 1W n = 7). g, The protein levels of p22phox, analyzed by western blotting with tubulin as loading control. h, The relative p22phox protein levels (n = 6). All bar graphs represent the mean ± s.e. Statistical significance was determined using one-way ANOVA with Tukey test (b, c and e) and unpaired Student’s t-test (two tailed) (e, f and h).
