Enhanced ERK-1/2 activation in mice susceptible to coxsackievirus-induced myocarditis
J. Clin. Invest. Mary Anne Opavsky, et al. 109:1561 doi:10.1172/JCI13971 [Go to this article.]

Figure 4
CVB3 replication in neonatal mouse cardiac myocyte cultures is regulated by Src’s and the ERK-1/2 signaling pathway. (a) Cardiac myocytes, isolated from neonatal mice, were incubated with DMSO (0) or the MEK-1/2 inhibitor UO126 for 1 hour at 37°C, infected with CVB3 (moi = 5), and then incubated for 48 hours. (b) Cardiac myocytes were incubated with DMSO (0) or the Src’s PP2 for 1 hour at 37°C, then infected as above. Virus titers are expressed as mean pfu/2 × 10⁵ cells (± SEM, n = 3 per group). *P < 0.05 DMSO versus kinase inhibitor for each cell type (ANOVA plus Bonferroni/Dunn post hoc testing). (c) ERK-1/2 activation following CVB3 infection in isolated cardiac myocytes was blocked by inhibition of ERK-1/2 and Src activation. The increase in ERK-1/2 phosphorylation observed 48 hours after viral infection was inhibited by treatment with 1 μM UO126 (UO) and 1 μM PP2. One result represents two experiments. Cell lysates were immunoblotted with anti–phospho-ERK-1/2 (P-ERK-1/2) and anti–total ERK-1/2 Ab’s. Fold change in P-ERK-1/2-total ERK-1/2 ratio is indicated.