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Unité d’Ontogénie et Reproduction (J.A.A., S.K.B., P.C., E.M., M.A.F.), Centre Hospitalier Universitaire de Québec, Centre Hospitalier de l’Université Laval, Centre de Recherche en Biologie de la Reproduction, and Département d’Obstétrique et Gynécologie, Université Laval (M.A.F.), Québec, G1K 704, Canada; and Centre de Recherche en Reproduction Animale (J.S.), Département de biomédecine vétérinaire, Université de Montréal, Québec J2S 7C6, Canada
Address all correspondence and requests for reprints to: Dr. Michel A. Fortier, Ph.D., Unité d’Ontogénie et Reproduction, Centre de Recherche du Centre Hospitalier Universitaire de Québec, Centre Hospitalier de l’Université Laval, 2705 Boul Laurier, Ste-Foy, Québec GIV 4G2, Canada. E-mail: mafortier{at}crchul.ulaval.ca.
The corpus luteum (CL) is a transient ovarian endocrine gland formed from the ovulated follicle. Progesterone is the primary secretory product of CL and is essential for establishment of pregnancy in mammals. In the cyclic female, the life span of CL is characterized by luteal development, maintenance, and regression regulated by complex interactions between luteotrophic and luteolytic mediators. It is universally accepted that prostaglandin (PG) F2a is the luteolysin whereas PGE2 is considered as a luteotropin in most mammals. New emerging concepts emphasize the autocrine and paracrine actions of luteal PGs in CL function. However, there is no report on selective biosynthesis and cellular transport of luteal PGE2 and PGF2
in the CL of any species. We have studied the expression of enzymes involved in the metabolism of PGE2 and PGF2, cyclooxygenase (COX)-1 and -2, PGE and F synthases, PG 15-dehydrogenase, and PG transporter as well as receptors (EP2, EP3, and FP) throughout the CL life span using a bovine model. COX-1, PGF synthase, and PG 15-dehydrogenase are expressed at constant levels whereas COX-2, PGE synthase, PG transporter, EP2, EP3, and FP are highly modulated during different phases of the CL life span. The PG components are preferentially expressed in large luteal cells. The results indicate that PGE2 biosynthesis, transport, and signaling cascades are selectively activated during luteal maintenance. By contrast the PGF2 system is activated during luteal regression. Collectively, our results suggest an integrated role for luteal PGE2 and PGF2 in autoregulation of CL function.
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