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. Author manuscript; available in PMC: 2010 Mar 9.
Published in final edited form as: J Cardiovasc Pharmacol. 2009 Jun;53(6):486–494. doi: 10.1097/FJC.0b013e3181a7b58a

FIGURE 2.

FIGURE 2

S1P-mediated ERK activation is PTX sensitive and requires MEK phosphorylation. Quiescent cardiomyocytes were pretreated or not for 16 hours with 100 ng/mL of the Gi/o inhibitor PTX (A) or for 1 hour with 10 μM of the MEK inhibitor PD98059 (B) before incubation with 100 nM S1P for 10 minutes. The phosphorylation of ERK 1/2 induced by S1P was abolished by PTX or PD98059. Equal gel loading was verified using an antibody against total ERK 1/2. Specific bands corresponding to phosphorylated forms of ERK 1/2 were quantified by densitometry and expressed as percentage of the corresponding control. Data are expressed as mean ± SEM of 3–4 independent experiments. *P < 0.05 compared with all other values. Veh, vehicle.