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. Author manuscript; available in PMC: 2008 Feb 26.
Published in final edited form as: J Mol Cell Cardiol. 2005 May;38(5):765–775. doi: 10.1016/j.yjmcc.2005.02.020

Fig. 4.

Fig. 4

Distinct signaling pathways are involved in ERK phosphorylation elicited by EGF or ONOO−. A. H9C2 cells were NS or treated with 0.1 μg ml−1 EGF for 15 min in the absence or in the presence of AG1478 (100 nM), BAY 43–9006 (5 μM) or PD98059 (50 μM). The phosphorylation of ERK 1/2 (p44/p42) induced by EGF was prevented by AG1478, BAY 43–9006 or PD98059. B. Cells were NS or treated with ONOO− (500 μM, 15′) with or without inhibitors. The activation of ERK 1/2 (p44/p42) induced by ONOO− was not influenced by AG1478, but was prevented by BAY 43–9006 and PD98059. Densitometric analyses are shown as mean ± S.E.M. of at least three independent experiments. * P < 0.05 vs. NS. † P < 0.05 vs. EGF. # P < 0.05 vs. ONOO−.