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. Author manuscript; available in PMC: 2011 May 18.
Published in final edited form as: Cell Cycle. 2010 Apr 15;9(8):1639–1646. doi: 10.4161/cc.9.8.11509

Figure 4.

Figure 4

Trypanosoma cruzi infection induces activation of ERK 1/2 in cultured cardiac myocytes and in the myocardium of infected mice. (A) Cultured cardiac myocytes were infected with T. cruzi and blots were probed against anti-total ERK and pERK. There was no change in total ERK over a 72 hours infection. However, a progressive increase in pERK (activation) over the same period of time was observed. GAPDH (36 KDa) was used as loading control in myocyte samples (n = 3 for each group). (C and D) Hearts obtained from Brazil strain infected mice (66 and 180 days post infection, dpi) were subjected to SDS-PAGE analysis and probed with anti-phosphoERK antibody. T. cruzi infection induced a 2.3-fold increase in pERK (activation) at 66 dpi and a 68% decrease at 180 dpi as compared with age-matched uninfected controls. BIP (78 KDa) was used as loading control for heart tissue samples (n = 4 for each group) (*p < 0.05, ANOVA).