Evidence for the involvement of Gi2 in activation of extracellular signal-regulated kinases in hepatocytes
1 Department of Pharmacology, Faculty of Medicine, University of Oslo, Box 1057 Blindern, N-0316, Oslo, Norway
2 Institute for Cancer Research, Department of Immunology, Molecular Medicine Group, The Norwegian Radium Hospital, Montebello, N-0310, Oslo, Norway
BMC Cell Biology 2001, 2:13 doi:10.1186/1471-2121-2-13Published: 24 July 2001
Activation of the extracellular signal-regulated kinases ERK1 and ERK2 in hepatocytes by prostaglandin (PG)F2α was recently found to be inhibited by pertussis toxin (PTX) suggesting a role for Gi proteins.
Targeting the Gi2α expression by a specific ribozyme inhibited the PGF2α -induced ERK1/2 activation in hepatocytes. On the other hand a non-cleaving form of the Gi2α ribozyme did not significantly decrease the ERK1/2 activation. In ribozyme-treated cells the Gi2α protein level was reduced, while the Gqα level was not affected thus confirming the specificity of the ribozyme.
The present data suggest an important role of Gi2 in PGF2α -induced ERK1/2 signaling in hepatocytes.