Myostatin upregulation following PE stress is Erk dependent via MEF-2.

<p>Cardiomyocytes were isolated from neonatal rats and grown to confluency. Cells were treated with small molecule inhibitors of PI3K (wortmannin, 5 nM), p38 (SB203580, 3 uM), Erk (PD98059, 50 uM), calcineurin (cyclosporine, 1 uM), or control 1 hour prior to 18 hours of PE stress (100 uM) and compared to baseline (no PE, no inhibition). Each condition was tested n = 4 times. (A) Western blot was performed to assess expression of the myostatin precursor protein using the C-terminus antibody. (B) The assay was repeated with the Erk inhibitor once it was identified as being the most potent inhibitor of myostatin expression to confirm results. (C) Western blot was performed on nuclear extracts to assess the levels of nuclear MEF-2. (D) EMSA was performed to assess MEF-2 DNA binding activity in nuclear extracts. #p<0.05 vs. PE (ANOVA); *p<0.05 vs. Con (ANOVA).