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. 2016 May 6;6:25372. doi: 10.1038/srep25372

Figure 7. STIM1 mutant mice exhibit a blunted response to pressure-overload-induced cardiac hypertrophy.

Figure 7

(A) Representative section of heart from STIM1 controls and STIM1 mutant. Left ventricular size was increased significantly in STIM1 control hearts. (B) Serial echocardiographic analysis and quantification of fractional shortening. (C) Postmortem ventricular weight/body weight ratio. Heart was harvested and ventricular weight is normalized for body weight. (D) Immunoblotting of isolated cardiomyocytes lysates blotted for STIM1, ERK1/2, activated ERK1/2 (pERK1/2) and GAPDH. (E) Quantitative analysis of four independent western blots, quantification was standardized relative to GAPDH signal, differences are reported in fold increase. (F) Summary of ELISA results from adult cardiomyocytes showing reduced p397-FAK in the STIM1 knockout cells, data were normalized for total FAK. (G) Representative immunoblotting of calcineurin (CnA), p-AKT (Ser473), AKT and total calmodulin dependent kinase II (CamKII) from heart lysates. (H) Same as in “panel G” but samples were extracted from mice after 14 days of TAC. (I) AKT densitometry results from multiple immunoblots, heart samples were harvested from mice after 14 days of TAC. Scale bar, 1.0 mm. Data are expressed as mean ± SEM, *P < 0.05.