title: Intraluteal regulation of prostaglandin F2 alpha-induced prostaglandin biosynthesis in pseudopregnant rabbits.
abstract: The objective of the present study was to investigate in rabbit corpora lutea (CL), at both the cellular and molecular level, intraluteal cyclooxygenase (COX)-1, COX-2 and prostaglandin (PG) E2-9-ketoreductase (PGE2-9-K) enzymatic activities as well as in vitro PGE2 and PGF2alpha synthesis following PGF2alpha treatment at either early- (day-4) or mid-luteal (day-9) stage of pseudopregnancy. By immunohistochemistry, positive staining for COX-2 was localized in luteal and endothelial cells of stromal arteries at both the stages. In CL of both stages, basal COX-2 mRNA levels were poorly expressed, but rose (P < 0.01) 4- to 10-fold 1.5-6 h after treatment and then gradually decreased within 24 h. Compared to mid-stage, day-4 CL had lower (P < 0.01) COX-2 and PGE2-9-K basal activities, and PGF2alpha synthesis rate, but higher (P < 0.01) PGE2 production. Independent of luteal stage, PGF2alpha treatment did not affect COX-1 activity. In day-4 CL, PGF2alpha induced an increase (P < 0.01) in both COX-2 activity and PGF2alpha synthesis, whereas that of PGE2 remained unchanged. In day-9 CL, PGF2alpha up-regulated (P < 0.01) both COX-2 and PGE-9-K activities, and PGF2alpha production, but decreased (P < 0.01) PGE2 synthesis. All changes in gene expression and enzymatic activities occurred within 1.5 h after PGF2alpha challenge and were more marked in day-9 CL. Our data suggest that PGF2alpha directs intraluteal PG biosynthesis in mature CL, by affecting the CL biosynthetic machinery to increase the PGF2alpha synthesis in an auto-amplifying manner, with the activation of COX-2 and PGE-9-K; this may partly explain their differentially, age-dependent, luteolytic capacity to exogenous PGF2alpha in rabbits.
authors.affiliation: Dipartimento di Biologia Molecolare, Cellulare e Animale, Università di Camerino, via F Camerini 1, Camerino, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Zerani
authors.forename: C
authors.initials: C
authors.lastname: Dall'Aglio
authors.forename: M
authors.initials: M
authors.lastname: Maranesi
authors.forename: A
authors.initials: A
authors.lastname: Gobbetti
authors.forename: G
authors.initials: G
authors.lastname: Brecchia
authors.forename: F
authors.initials: F
authors.lastname: Mercati
authors.forename: C
authors.initials: C
authors.lastname: Boiti
mesh_terms: D000818:Animals; D003338:Corpus Luteum / Q000187:drug effects / Q000378:metabolism*; D051545:Cyclooxygenase 1 / Q000096:biosynthesis; D051546:Cyclooxygenase 2 / Q000096:biosynthesis; D015237:Dinoprost / Q000096:biosynthesis / Q000494:pharmacology*; D015232:Dinoprostone / Q000032:analysis / Q000096:biosynthesis*; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D006911:Hydroxyprostaglandin Dehydrogenases / Q000032:analysis / Q000378:metabolism; D003341:Luteolysis; D011374:Progesterone / Q000032:analysis; D011555:Pseudopregnancy / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D011817:Rabbits; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D015854:Up-Regulation
chemical_list: D012333:RNA, Messenger; D011374:Progesterone; D015237:Dinoprost; D006911:Hydroxyprostaglandin Dehydrogenases; C035858:prostaglandin-E2 9-reductase; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D015232:Dinoprostone