RGD Reference Report - ERK2 mediates oxytocin-stimulated PGE2 synthesis. - Rat Genome Database
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ERK2 mediates oxytocin-stimulated PGE2 synthesis.

Authors: Strakova, Z  Copland, JA  Lolait, SJ  Soloff, MS 
Citation: Strakova Z, etal., Am J Physiol. 1998 Apr;274(4 Pt 1):E634-41.
RGD ID: 2304227
Pubmed: (View Article at PubMed) PMID:9575824

Oxytocin (OT) induces PG synthesis by both uterine endometrial and amnion cells. We showed previously that CHO cells stably transfected with the rat oxytocin receptor (CHO-OTR cells) also synthesize PGE2 in response to OT. In the present work we have demonstrated that OTRs are coupled to both Gi and Gq/11, using immunoprecipitation of solubilized OTR complexes and ADP ribosylation. OT treatment caused the rapid phosphorylation of extracellular signal-regulated protein kinase 2 (ERK2 or p42MAPK), which was partially inhibited by pertussis toxin (PTX), consistent with OTR-Gi coupling. The PTX-insensitive portion of ERK2 phosphorylation was linked to Gq, as inhibitors of both phospholipase C (U-73122) and protein kinase C (GF-109203X) blocked OT-induced ERK2 phosphorylation. OT-stimulated c-fos expression was also mediated by ERK2 phosphorylation. The ERK-c-fos pathway has been shown to be associated with cell proliferation, but OT had no effect on [3H]thymidine uptake by CHO-OTR cells. However, inhibition of OT-induced ERK2 phosphorylation with an ERK kinase inhibitor (PD-98059) markedly reduced OT-stimulated PGE2 synthesis, pointing to the importance of ERK2 activation in OT action.

Annotation

Gene Ontology Annotations    

Biological Process

Molecular Pathway Annotations    
Objects Annotated

Genes (Rattus norvegicus)
Oxt  (oxytocin/neurophysin I prepropeptide)
Oxtr  (oxytocin receptor)


Additional Information