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. Author manuscript; available in PMC: 2015 Sep 1.
Published in final edited form as: J Mol Cell Cardiol. 2014 May 5;74:76–87. doi: 10.1016/j.yjmcc.2014.04.020

Fig. 7.

Fig. 7

Effect of the TRAF6 inhibitory peptide and control peptide on lipopolysaccharide (LPS)-induced cardiomyocyte contractile defects. Freshly isolated cardiomyocytes from WT or akt2 knockout (AKO) mice were incubated with LPS (1 µg/ml) in the presence or absence of TRAF6 inhibitory peptide (300 µM) or control peptide (300 µM) for 4 hrs. A: Resting cell length; B: Peak shortening (normalized to resting cell length); C: Maximal velocity of shortening (+ dL/dt); D: Maximal velocity of relengthening (− dL/dt); E: Time-to-peak shortening (TPS) and F: Time-to-90% relengthening (TR90). Mean ± SEM, n = 62 cells per group, * p < 0.05 vs. WT group, # p < 0.05 vs. WT-LPS group.