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*12-O-TETRADECANOYLPHORBOL-13-ACETATE
*PROSTAGLANDIN F2ALPHA
Endocrinology Vol. 142, No. 2 887-895
Copyright © 2001 by The Endocrine Society

ARTICLES

Induction of c-fos and c-junMessenger Ribonucleic Acid Expression by Prostaglandin F2{alpha} Is Mediated by a Protein Kinase C-Dependent Extracellular Signal-Regulated Kinase Mitogen-Activated Protein Kinase Pathway in Bovine Luteal Cells1

Dongbao Chen2, Hon Wa Fong and John S. Davis

The Women’s Research Institute (D.C., H.W.F., J.S.D.), Departments of Obstetrics and Gynecology, and Internal Medicine, University of Kansas School of Medicine-Wichita, and Research Service of the Department of Veterans Affairs (J.S.D.), 1010 North Kansas, Wichita, Kansas 67214

Address all correspondence and requests for reprints to: John S. Davis, Ph.D., The Women’s Research Institute, 1010 North Kansas, Wichita, Kansas 67214-3199. E-mail: jdavis3{at}kumc.edu

PGF2{alpha} triggers the demise of the corpus luteum whereby progesterone synthesis is inhibited, the luteal structure regresses, and the estrus cycle resumes. Upon binding to its heterotrimeric G-protein-coupled receptors, PGF2{alpha} initiates the phospholipase C/diacylglycerol and inositol-1,4,5-trisphosphate/Ca2+-protein kinase C (PKC) signaling pathway. More recently, we have demonstrated that PGF2{alpha} activates extracellular signal-regulated kinase (ERK) mitogen-activated protein (MAP) kinase signaling through a Raf-dependent mechanism in bovine luteal cells. However, the relationship between PKC and ERK activation in PGF2{alpha} signaling has not been clearly defined. Moreover, the signaling pathway that PGF2{alpha} uses to regulate gene expression is unknown. In this report, primary cultures of bovine luteal cells were used to address the role of PKC in ERK activation and the signaling pathway for induction of c-fos and c-jun messenger RNA (mRNA) expression in response to PGF2{alpha}. By using a PKC inhibitor and a PKC-deficient luteal cell model, we observed that phorbol ester-responsive isoforms of PKC were required for ERK phosphorylation and activation by PGF2{alpha} (1 µM) or phorbol 12-myristate 13-acetate (PMA) (20 nM). In PGF2{alpha}- and PMA-treated cells, active ERK MAP kinase was localized in the nucleus. PGF2{alpha}-induced ERK phosphorylation was dose-dependently inhibited by the MEK1 inhibitor PD098059 (1–50 µM). The expression of c-fos and c-jun mRNA in luteal cells was markedly increased by treatment with PGF2{alpha} (1 µM) or PMA (20 nM) for 30 min. We also observed that activation of ERK MAP kinase was required for the expression of c-fos and c-jun mRNA in response to PGF2{alpha} and PMA because it was abrogated by blocking the ERK pathway with PD098059. In addition, PGF2{alpha} and PMA-induced c-fos and c-jun mRNA expression was abolished in the PKC-deficient cells. Taken together, our data demonstrate that a PKC-dependent ERK MAP kinase pathway mediates the expression of c-fos and c-jun mRNA in PGF2{alpha}-treated bovine luteal cells.




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