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J. Biol. Chem., Vol. 278, Issue 14, 12151-12156, April 4, 2003
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From the Department of Pharmacology and Toxicology, College of
Pharmacy, University of Arizona, Tucson, Arizona 85721-0207
Prostaglandin E2
(PGE2) mediates its physiological effects by interactions
with a subfamily of G-protein-coupled receptors known as EP receptors.
These receptors consist of four primary subtypes named EP1,
EP2, EP3, and EP4. The
EP2 and EP4 subtypes are known to couple to
G
Prostaglandin E2 Induced Functional Expression of
Early Growth Response Factor-1 by EP4, but Not
EP2, Prostanoid Receptors via the Phosphatidylinositol
3-Kinase and Extracellular Signal-regulated Kinases*
s and stimulate intracellular cyclic 3,5- adenosine
monophosphate formation, whereas the EP1 and
EP3 receptors are known to couple to
Gq and Gi, respectively. Recently we found that EP2 and EP4 receptors can
activate T-cell factor signaling; however, EP2 receptors
did this primarily through a cAMP-dependent protein
kinase-dependent pathway, whereas EP4 receptors primarily utilized a phosphatidylinositol 3-kinase
(PI3K)-dependent pathway (Fujino, H., West, K. A., and
Regan, J. W. (2002) J. Biol. Chem. 277, 2614-2619). We now report that PGE2 stimulation of EP4 receptors, but not EP2 receptors, leads to
phosphorylation of the extracellular signal-regulated kinases (ERKs)
through a PI3K-dependent mechanism. Furthermore, this
activation of PI3K/ERK signaling by the EP4 receptors
induces the functional expression of early growth response factor-1
(EGR-1). Under the same conditions induction of EGR-1 protein
expression was not observed following PGE2 stimulation of
EP2 receptors. These findings point to important differences in the signaling potential of the EP2 and
EP4 receptors, which could be significant with respect to
the potential involvement of EP4 receptors in inflammation
and cancer.
*
This work was supported in part by Grant EY11291 from the
National Institutes of Health, Allergan Inc., and the Arizona Disease Control Research Commission.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed. Tel.: 520-626-2181;
Fax: 520-626-2466; E-mail: regan@pharmacy.arizona.edu.
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