Skip to main content
. Author manuscript; available in PMC: 2019 Jun 1.
Published in final edited form as: Metabolism. 2018 Mar 9;83:256–270. doi: 10.1016/j.metabol.2018.03.004

Figure 2. AMPK inactivation augments JNK activation during hypoxia and reoxygenation.

Figure 2

Figure 2

(A) H9c2 cells were treated with compound C (10 μM) and JNK-IN-8 (1 μM) under normoxia, hypoxia and hypoxia/reoxygenation. Upper: Immunoblotting showed phosphorylation of AMPK and downstream ACC, and phosphorylation of JNK and downstream c-Jun in H9c2 cells with or without AMPK inhibitor compound C and JNK inhibitor JNK-IN-8 under normoxia, hypoxia, and hypoxia/reoxygenation conditions; Lower: quantitative analysis of the relative levels of p-AMPK, p-ACC, p-JNK, and p-c-Jun in H9c2 cells with or without AMPK inhibitor or JNK inhibitor under normoxia, hypoxia, and hypoxia/reoxygenation. Values are mean ± SEM. N=4, *p<0.05 vs. normoxia, respectively; †p<0.05 vs. hypoxia vehicle; #p<0.05 vs. hypo/reoxy vehicle. (B) AMPKα1/α2 siRNA knockdown AMPKα catalytic subunit and JNK1/2 siRNA knockdown JNK1/2 in the H9c2 myoblast cells under normoxia, hypoxia, and hypoxia/reoxygenation. Upper: Immunoblotting showed phosphorylation of AMPK and downstream ACC, and phosphorylation of JNK and downstream c-Jun in H9c2 cells with or without AMPKα1/α2 siRNA and JNK1/2 siRNA under normoxia, hypoxia, and hypoxia/reoxygenation conditions; Lower: quantitative analysis of the relative levels of p-AMPK, p-ACC, p-JNK, and p-c-Jun in H9c2 cells with or without AMPKα1/α2 siRNA and JNK1/2 siRNA under normoxia, hypoxia and hypoxia/reoxygenation conditions. Values are mean ± SEM. N=3, *p<0.05 vs. normoxia, repectively; †p<0.05 vs. hypoxia scram; #p<0.05 vs. hypo/reoxy scram.