Evidence for the involvement of G(i2) in activation of extracellular signal-regulated kinases in hepatocytes

BACKGROUND: Activation of the extracellular signal-regulated kinases ERK1 and ERK2 in hepatocytes by prostaglandin (PG)F(2α) was recently found to be inhibited by pertussis toxin (PTX) suggesting a role for G(i) proteins. RESULTS: Targeting the Gi(2α) expression by a specific ribozyme inhibited the PGF(2α) -induced ERK1/2 activation in hepatocytes. On the other hand a non-cleaving form of the Gi(2α) ribozyme did not significantly decrease the ERK1/2 activation. In ribozyme-treated cells the Gi(2α) protein level was reduced, while the G(qα) level was not affected thus confirming the specificity of the ribozyme. CONCLUSION: The present data suggest an important role of G(i2) in PGF(2α) -induced ERK1/2 signaling in hepatocytes.