Alghough it is well established that exercise increases the binding of MEF2A to its cis-element on the GLUT4 promoter and GLUT4 expression, little is known about the intracellular signaling pathways involved in eliciting this response. The role of AMPKa 2 in regulating the exercise induced MEF2A nucleus translocation, MEF2A binding to the Glut4 promoter, and Glut4 expression was investigated in the present study. This was investigated in muscles from AMPKα2 over-expression (OE) mice, AMPKα2 knockout (KO) mice and corresponding wild-type (WT) mice that had undertaken a 28-days program of treadmill training.1) AMPKα-Thr172 phosphorylation by western blot.2) Total and nuclear MEF2A by western bolt.3) Bound MEF2A at the GLUT4 MEF2 cis-element by CHIP.4) GLUT4 expression by Real Time-PCR and Western blot. Over-expression of the AMPKα2 isofurm heightened the training-induced increase in nuclear MEF2A content, MEF2A binding to the Glut4 promoter and GLUT4 expression, and that the training-induced increases of Glut4 promoter-bound MFF2A and GLUT4 expression were normal inα2-KO muscles despite the reduced AMPK signaling, nuclear MEF2 content, suggest that AMPKa 2 is involved, though not indispensable, in regulating training-induced MEF2A binding to the Glut4 promoter and GLUT4 expression in skeletal muscle.
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