title: Peroxisome proliferator activated receptor ligands affect progesterone and 17β-estradiol secretion by porcine corpus luteum during early pregnancy.
abstract: In the present study we investigated the effect of peroxisome proliferator activated receptor (PPAR) ligands on progesterone (P4) and 17β-estradiol (E2) secretion and 3b-hydroxysteroid dehydrogenase/Δ(5)-Δ(4) isomerase (3β-HSD) mRNA abundance in porcine corpora lutea (CL) collected on days 10-12 and 14-16 of the estrous cycle or pregnancy. The PPAR agonists reduced P4 secretion by the CL during pregnancy whereas they were ineffective during the estrous cycle. An inhibitory effect of WY-14643 (PPARα agonist) on P4 release was noted on days 14-16 of pregnancy. The treatment of the CL with L-165,045 (PPARβ agonist) diminished P4 release by the tissue during both stages of pregnancy. A natural PPARγ agonist, PGJ2, reduced P4 release on days 14-16 or days 10-12 of pregnancy, respectively. Rosiglitazone (PPARγ agonist) inhibited P4 secretion by the CL on days 10-12 of pregnancy. In turn, PPARα ligands effect on E2 release was differential. While PPARγ activator diminished E2 secretion by the CL explants during all tested stages of the estrous cycle and pregnancy, PPARβ ligands did not induce any change in E2 level. In turn, PPARβ agonist reduced E2 release by the tissue during both stages of pregnancy but did not affect the secretion during the estrous cycle. In the present study there was a lack of PPAR ligands effect on 3β-HSD mRNA abundance. In summary, the results suggest that PPARs are involved in the regulation of progesterone and 17β-estradiol release by porcine CL. Porcine CL indicates a different receptivity to PPAR ligands depending on the reproductive status of animals.
authors.affiliation: Department of Animal Physiology, University of Warmia and Mazury in Olsztyn, Olsztyn, Poland. iwonab@uwm.edu.pl.
authors.forename: A
authors.initials: A
authors.lastname: Kurzynska
authors.forename: M
authors.initials: M
authors.lastname: Bogacki
authors.forename: K
authors.initials: K
authors.lastname: Chojnowska
authors.forename: I
authors.initials: I
authors.lastname: Bogacka
mesh_terms: D015096:3-Hydroxysteroid Dehydrogenases / Q000235:genetics; D000813:Anilides / Q000494:pharmacology; D000818:Animals; D001549:Benzamides / Q000494:pharmacology; D003338:Corpus Luteum / Q000187:drug effects / Q000378:metabolism*; D004958:Estradiol / Q000378:metabolism*; D030762:Estrous Cycle / Q000378:metabolism; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D007211:Indoles / Q000494:pharmacology; D008024:Ligands; D047492:Peroxisome Proliferator-Activated Receptors / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*; D010642:Phenoxyacetates / Q000494:pharmacology; D011247:Pregnancy; D011374:Progesterone / Q000378:metabolism*; D015230:Prostaglandin D2 / Q000031:analogs & derivatives / Q000494:pharmacology; D011725:Pyridines / Q000494:pharmacology; D011743:Pyrimidines / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D000077154:Rosiglitazone; D013552:Swine; D045162:Thiazolidinediones / Q000494:pharmacology; D002722:Chlorobenzenes
chemical_list: D015096:3-Hydroxysteroid Dehydrogenases; D000813:Anilides; D001549:Benzamides; D004958:Estradiol; D007211:Indoles; D008024:Ligands; D047492:Peroxisome Proliferator-Activated Receptors; D010642:Phenoxyacetates; D011374:Progesterone; D015230:Prostaglandin D2; D011725:Pyridines; D011743:Pyrimidines; D012333:RNA, Messenger; D000077154:Rosiglitazone; D045162:Thiazolidinediones; C457499:2-chloro-5-nitrobenzanilide; C520164:4-(3-(2-propyl-3-hydroxy-4-acetyl)phenoxy)propyloxyphenoxy acetic acid; C458508:T 0070907; C060893:MK-886; D002722:Chlorobenzenes; C037112:9-deoxy-delta-9-prostaglandin D2; C006253:pirinixic acid