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. 2017 May 23;595(13):4227–4243. doi: 10.1113/JP274030

Figure 6. Chronic leptin treatment reduces the TAC‐induced CaMKII activation and RyR2 phosphorylation.

Figure 6

A and B, representative immunoblots (top) and average ratio of protein levels (bottom), expressed as a percentage of p‐CaMKII (Thr286) of the total CaMKII in (A) and p‐RyR2 (Ser2814) normalized by the total RyR2 (B) in hearts (n = 3 or 4 mice) from sham and TAC mice treated either with vehicle or with leptin. C, representative line‐scan images presenting Ca2+ sparks recorded in cardiomyocytes from sham (left two panels) and TAC (right two panels) mice treated either with vehicle or with leptin, as indicated in the labels below each image. Average Ca2+ spark frequency per second and per 100 μm (D), their amplitude as peak F/F 0 (E) and Ca2+ spark frequency per second and per 100 μm normalized to SR load measured as F/F 0 (F) in each group studied (n = 4–6 mice; n = 50–70 cells). Data are the mean ± SEM. * P < 0.05, ** P < 0.01 and *** P < 0.001 vs. sham vehicle; P < 0.05 and ††† P < 0.001 vs. TAC vehicle; # P < 0.05 and ### P < 0.001 vs. sham leptin.