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. Author manuscript; available in PMC: 2018 Jan 1.
Published in final edited form as: Basic Res Cardiol. 2017 May 22;112(4):38. doi: 10.1007/s00395-017-0628-z

Figure 6. Activation of ERK1/2 and HSP27 is essential for the anti-apoptotic effect of exercise-derived extracellular vesicles in cardiomyocytes.

Figure 6

(a and c) Inhibition of ERK1/2 via PD98059 reduced ERK1/2 and HSP27 phosphorylation level in H9C2 cells (n=3). (b and d) Inhibition of HSP27 via SB203580 reduced HSP27 but not ERK1/2 phosphorylation level, confirming HSP27 as a downstream effector of ERK1/2 (n=3). (e) Flow cytometry showed that inhibition of ERK1/2 or HSP27 abolished the anti-apoptotic effect of exercise-induced increase of EVs in H2O2-treated H9C2 cells (n=5). EVs, extracellular vesicles. *, P<0.05 vs. Control group; #, P<0.05 vs. 1.85 Swim group.