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. Author manuscript; available in PMC: 2013 Oct 23.
Published in final edited form as: Circulation. 2012 Sep 27;126(17):2095–2104. doi: 10.1161/CIRCULATIONAHA.111.071480

Figure 6. AAV9.SERCA2a gene transfer reverses increased RyR2 Po in heart failure.

Figure 6

Panel A. Measurement of the slope of optically-recorded Ca2+ tracings during diastole, immediately following the last paced beat (CL 130-150 ms) as a marker of spontaneous diastolic SR Ca2+ release (i.e. RyR Po). As demonstrated, spontaneous diastolic SR Ca2+ release increased (i.e. increased RyR Po) in heart failure when compared to control. SERCA2a gene transfer in HF decreased spontaneous diastolic SR Ca2+ release when compared to HF alone and was similar to control. Panel B: In normal hearts, we observed a similar increase and decrease in spontaneous diastolic SR Ca2+ in response to treatment with caffeine (increasing RyR Po) and ryanodine (decreasing RyR2 Po), respectively. *p<0.01 by ANOVA. Panel C: CaMKII RyR phosphorylation (RyR-PS2814) in control (n=3), heart failure (n=3) and heart failure + AAV9.SERCA2a gene transfer (n=4). As shown, RyR-PS2814 increased in HF when compared to control and AAV9.SERCA2a gene transfer in the failing heart decreased RyR-PS2814 (p<0.05 by ANOVA).