Fig. 8.
Effects of BMAL1 deletion and/or SR-9009 administration on contractile function, markers of hypertrophy, and markers/mediators of fibrosis. Cardiomyocyte-specific BMAL1-knockout (CBK) and littermate control (CON) mice were challenged with either SR-9009 (SR; 100 mg·kg−1·day−1 ip) or vehicle (Veh) at zeitgeber time (ZT)9 for 8 consecutive days, followed by heart isolation 6 h after the last administration (i.e., ZT15). A: assessment of contractile function parameters in isolated working mouse hearts: cardiac power (i) and rate pressure product (ii). B: cardiomyocyte area assessment by wheat germ agglutinin (WGA) staining (i and ii). C: assessment of anf (i) and mhcβ (ii) expression by RT-PCR. D: interstitial fibrosis assessment by Picrosirius Red staining (i and ii). E: assessment of phosphorylated ERK1/2 (pERK1/2; i and ii), total ERK1/2 (ERK1/2; i and iii), and the phospho-to-total ratio (pERK1/2/ERK1/2; iv). F: assessment of phosphorylated SMAD3 (pSMAD; i and ii), total SMAD3 (SMAD3; i and iii), and the phospho-to-total ratio (pSMAD/SMAD3; iv). Data are reported as means ± SE for 7–14 mice/experimental group. Main effects for SR, genotype, and/or interaction are reported at the top of each graph. *P < 0.05 for CON (●) vs. CBK (red squares) within a treatment group; $P < 0.05 for vehicle vs. SR administration within a genotype; #P = 0.075 for vehicle vs. SR administration within a genotype.