title: Prostaglandin receptors and role of G protein-activated pathways on corpora lutea of pseudopregnant rabbit in vitro.
abstract: Studies were conducted to characterize receptors for prostaglandin (PG) F(2alpha) (PGF(2alpha)) and PGE(2), and the signalling pathways regulating total nitric oxide synthase activity and progesterone production in rabbit corpora lutea (CL) of different luteal stages. CL were obtained at days 4, 9 and 13 of pseudopregnancy and cultured in vitro for 2 h with PGF(2alpha) or PGE(2) and with activators and inhibitors of G protein (Gp), phospholipase C (PLC), protein kinase C (PKC), adenylate cyclase (AC) and protein kinase A (PKA). High affinity PGF(2alpha) receptor (K(d)=1.9+/-0.6 nM mean+/-s.e.m. ) concentrations increased (P< or =0.01) four- to five-fold from early to mid- and late-luteal phases (50.6+/-8.5, 188.3+/-36.1 and 231.4+/-38.8 fmol/mg protein respectively). By contrast, PGE(2) receptor (K(d)=1.6+/-0.5 nM) concentrations decreased (P< or =0.01) from day 4 to day 9 and 13 (27.5+/-7.7, 12.4+/-2.4 and 16.5+/-3.0 fmol/mg protein respectively). The Gp-dependent AC/PKA pathway was triggered only on day 4 CL, mimicking the PGE(2) treatment and increasing progesterone production. In both day 9 and day 13 CL, the Gp-activated PLC/PKC pathway evoked a luteolytic effect similar to that induced by PGF(2alpha). The time-dependent selective resistance to PGF(2alpha) and PGE(2) by rabbit CL is mediated by factors other than a lack of luteal receptor-ligand interactions.
authors.affiliation: Dipartimento di Patologia, Diagnostica e Clinica veterinaria, Università di Perugia, Via S. Costanzo 4, I-016126 Perugia, Italy. cboiti@unipg.it
authors.forename: C
authors.initials: C
authors.lastname: Boiti
authors.forename: D
authors.initials: D
authors.lastname: Zampini
authors.forename: M
authors.initials: M
authors.lastname: Zerani
authors.forename: G
authors.initials: G
authors.lastname: Guelfi
authors.forename: A
authors.initials: A
authors.lastname: Gobbetti
mesh_terms: D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000262:Adenylyl Cyclases / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D005576:Colforsin / Q000494:pharmacology; D003338:Corpus Luteum / Q000378:metabolism*; D046508:Culture Techniques; D015237:Dinoprost / Q000378:metabolism / Q000494:pharmacology*; D015232:Dinoprostone / Q000378:metabolism / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D019206:GTP-Binding Protein alpha Subunits, Gi-Go / Q000494:pharmacology; D019204:GTP-Binding Proteins / Q000494:pharmacology*; D007099:Imipramine / Q000494:pharmacology; D008183:Luteal Phase / Q000378:metabolism*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D011374:Progesterone / Q000032:analysis / Q000096:biosynthesis; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism; D011555:Pseudopregnancy; D011817:Rabbits; D011982:Receptors, Prostaglandin / Q000378:metabolism*; D018078:Receptors, Prostaglandin E / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*; D018709:Statistics, Nonparametric; D019311:Staurosporine / Q000494:pharmacology; D010738:Type C Phospholipases / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D011982:Receptors, Prostaglandin; D018078:Receptors, Prostaglandin E; D005576:Colforsin; D015124:8-Bromo Cyclic Adenosine Monophosphate; D011374:Progesterone; D015237:Dinoprost; D019001:Nitric Oxide Synthase; D011493:Protein Kinase C; D010738:Type C Phospholipases; D019204:GTP-Binding Proteins; D019206:GTP-Binding Protein alpha Subunits, Gi-Go; D000262:Adenylyl Cyclases; D019311:Staurosporine; D015232:Dinoprostone; D007099:Imipramine; D019331:NG-Nitroarginine Methyl Ester