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. Author manuscript; available in PMC: 2017 May 24.
Published in final edited form as: Circulation. 2016 Apr 8;133(21):2038–2049. doi: 10.1161/CIRCULATIONAHA.115.020226

Figure 8.

Figure 8

Inhibition of BCKDK by BT2 promotes BCKA degradation and preserves cardiac function in pressure-overloaded heart. A, Immunoblot for total and phosphorylated BCKD subunit E1α in heart from wildtype mice treated with vehicle (veh, n=4) or with BT2 (n=5). B, The average phosphorylation level of E1α vs. total E1α are presented with SEM. Error bars represent SEM, *, p < 0.05 between Veh and BT2 treated samples. C, BCKD activity in cardiac tissues from wildtype or PP2Cm-KO mice treated with vehicle or BT2 (n=4–5 in each group). *, p < 0.05 between Veh and BT2 treated groups. D, Individual BCKA concentration in plasma from wildtype and PP2Cm-KO (n=4–6) mice treated with vehicle (veh group) or with BT2 (BT2 group).*, p<0.05 between Veh and BT2 treated groups of same genotype. E, Representative M-mode echocardiographs of mouse hearts following sham or post-TAC treated with vehicle (Veh) or BT2. F, Left ventricular Ejection Fraction (%LVEF, n=6–8), and G, left ventricular internal dimension at systole (LVIDs, n=6–8) from mice with sham or TAC surgery for 4 weeks, treated with or without BT2 as indicated. Error bars represent SEM., *, p< 0.05 between designated groups.