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. Author manuscript; available in PMC: 2015 Dec 5.
Published in final edited form as: Circ Res. 2014 Oct 20;115(12):976–985. doi: 10.1161/CIRCRESAHA.116.304475

Figure 2. GRK5 Enhances NFAT Transcriptional Activity In Vivo in Models of Cardiac Pathology.

Figure 2

(A) Ex vivo NFAT luciferase assay from whole heart of NFAT-luciferase reporter mice with concomitant GRK5 overexpression (TgGRK5/LUC) or littermates with endogenous levels of GRK5 (LUC). Hearts were removed from 8-12 week old mice. (LUC n=6, TgGRK5/LUC n=8. *,p<0.05 by t-test). (B) Ejection fraction was determined by echocardiography in TgGRK5/LUC or LUC littermates with endogenous levels of GRK5 2 weeks after transaortic constriction (TAC) or sham surgery (SHAM). (C) Ex vivo NFAT luciferase assay from whole heart of TgGRK5/LUC or LUC littermates after TAC. (D) Quantitative RT-PCR for NFAT target gene RCAN from whole heart of NFAT luciferase reporter mice. (LUC SHAM n=10, LUC TAC n=13, TgGRK5/LUC SHAM n=17, TgGRK5/LUC TAC n=17. **,p<0.01; ***,p<0.001 by ANOVA). (E) Ex vivo NFAT luciferase assay from whole heart of TgGRK5/LUC mice or LUC littermates after 24 hours of PE administration (35 mg/kg/day). (LUC PBS n=9, LUC PE n=7, TgGRK5/LUC PBS n=11, TgGRK5/LUC PE n=15. **,p<0.01; ***,p<0.001 by ANOVA).