FIGURE 7.

LPI mediated ERK1/2 phosphorylation in U2OS cells containing GPR55E. A, GPR55E cells treated for 10 min with 3 and 10 μm LPI demonstrated ERK1/2 activation significantly different from vehicle-treated cells (*, p < 0.05; **, p < 0.001). Co-application of 10 μm CP55,940 significantly inhibited 10 μm LPI-mediated ERK1/2 activation. In contrast, 10 μm CP55,940 (CP)-, 30 μm SR141716A (SR)-, and AM251 (AM)-mediated ERK activation was not different from vehicle treatment. The data represent the mean ± S.E. from at least three independent experiments performed in duplicate. B, 10 μm LPI fails to evoke ERK1/2 activation in untransfected U2OS cells, whereas activation of ERK occurs with 1 mm pervanadate treatment. C, in U2OS cells stably expressing the CB₁RE, 10 μm LPI failed to activate ERK1/2, whereas treatment with 10 μm CB₁ agonist, CP 55,940, resulted in a marked increase of ERK1/2 activation.