Extended Data Fig. 1: AAV9-mediated SERCA2a overexpression rescues SERCA2a levels and ejection fraction in p22phox cKO mice.
From: p22phox prevents the oxidation of SERCA2a and stabilizes it in the heart
(a–g) Control and p22phox cKO mice were injected with adeno-associated virus 9 (AAV9) that harbors either GFP or SERCA2a under cTnT promoter one week prior to sham or TAC surgery. Post-surgery the mice were sacrificed at 4-week time point and the following analyses were conducted (a) Representative immunoblots showing SERCA2a levels with GAPDH as loading control in control and p22phox cKO mice under sham group with adeno-associated virus 9 (AAV9) that harbors either GFP or SERCA2a. (b) Relative SERCA2a to GAPDH ratio in (A) (n = 6). (c) Representative immunoblots showing SERCA2a levels with GAPDH as loading control in p22phox cKO mice under sham and TAC (4 W) condition with adeno-associated virus 9 (AAV9) that harbors either GFP or SERCA2a. (d) Quantification of SERCA2a to GAPDH ratio in (C) (n = 6). (e) Left ventricle weight to tibia length ratio (LVW/TL ratio) in control and p22phox cKO mice under sham and TAC(4 W) condition with adeno-associated virus 9 (AAV9) that harbors either GFP or SERCA2a (n = 6). (f) Lung congestion measured as lung weight to tibia length ratio (Lung W/TL ratio) in control and p22phox cKO mice under sham and TAC(4 W) condition with adeno-associated virus 9 (AAV9) that harbors either GFP or SERCA2a (n = 6). (g) Left ventricle ejection fraction % (LVEF%) measured by echocardiography in control and p22phox cKO mice under sham and TAC(4 W) condition with adeno-associated virus 9 (AAV9) that harbors either GFP or SERCA2a (n = 6). All bar graphs are represented as Mean ± SE. The statistical significance was determined with 1-way ANOVA with Tukey test (B, D and F-G) and 1-way ANOVA with Å Ãdák’s multiple comparisons test (e).
