Fig. 4.

Fg-induced ERK-1/2 activation is partially a result of endothelin-1 (ET-1) production (mediated by endothelin-converting enzyme), which binds to endothelin type B receptors on ECs. A and C: examples of Fg (4 mg/ml)- and ET-1 (10⁻⁸ M)-induced phosphorylation of ERK-1/2 shown by Western blot analysis. The endothelin type B receptor blocker BQ-788 (1 μM) decreased Fg-induced ERK-1/2 phosphorylation and abolished ET-1-induced phosphorylation of ERK-1/2; n = 9 (A). The endothelin-converting enzyme inhibitor SM-19712 (0.2 mM) decreased Fg-induced ERK-1/2 phosphorylation, whereas endothelin type A receptor blocker BQ-123 (1 μM) did not; n = 3 (C). B and D: densitometric analysis of ERK-1/2 signal. Data are presented as a ratio of IOD of phosphorylated ERK-1/2 bands to the IOD of bands of the corresponding total ERK-1 protein. *P < 0.05 vs. control, †P < 0.05 vs. Fg, #P < 0.05 vs. ET-1, ‡P < 0.05 vs. Fg + BQ-788.