title: In vitro effect of peroxisome proliferator activated receptor (PPAR) ligands on prostaglandin E2 synthesis and secretion by porcine endometrium during the estrous cycle and early pregnancy.
abstract: Peroxisome proliferator activated receptors (PPARs) are ligand-dependent transcriptional factors which are expressed in distinct tissues of the female reproductive system, including the ovary, uterus and placenta. An important role of PPARs in the regulation of reproductive processes has been previously highlighted in rodents. In the present study we investigated the in vitro effect of PPAR ligands on prostaglandin E2 (PGE2) release and prostaglandin E synthase (PGES) gene expression in the endometrial explants collected from cyclic (days 10-12 and 14-16 of the estrous cycle) or pregnant (days 10-12 and 14-16) pigs. A stimulatory (p<0.05) effect of rosiglitazone (PPARγ agonist) on PGE2 accumulation was noted during both stages of the estrous cycle and both stages of pregnancy, whereas a higher (p<0.05) PGES mRNA level was observed on days 10-12 of the estrous cycle and on days 14-16 of gestation when compared to the controls. The activation of PPARβ by L-165,041 augmented (p<0.05) PGE2 release by the endometrium on days 14-16 of the estrous cycle and on days 14-16 of pregnancy, but the increase (p<0.05) in PGES mRNA abundance was noted on days 10-12 of the estrous cycle and during both stages of pregnancy. A stimulatory (p<0.05) effect of WY-14643 (agonist) and MK 886 (antagonist) on PGE2 release was noted on days 10-12 of the estrous cycle, and days 14-16 of pregnancy, respectively. There was a lack of change in PGES mRNA abundance in the endometrium exposed to PPARα ligands. We conclude that PPARs are mediators of prostaglandin E2 synthesis/accumulation in porcine endometrium during the luteal phase of the estrous cycle and the time of periimplantation.
authors.affiliation: Department of Animal Physiology, University of Warmia and Mazury in Olsztyn, Olsztyn, Poland. iwonab@uwm.edu.pl
authors.forename: I
authors.initials: I
authors.lastname: Bogacka
authors.forename: M
authors.initials: M
authors.lastname: Bogacki
authors.forename: M
authors.initials: M
authors.lastname: Gaglewska
authors.forename: A
authors.initials: A
authors.lastname: Kurzynska
authors.forename: M
authors.initials: M
authors.lastname: Wasielak
mesh_terms: D000818:Animals; D015232:Dinoprostone / Q000819:agonists / Q000037:antagonists & inhibitors / Q000096:biosynthesis* / Q000378:metabolism; D004717:Endometrium / Q000187:drug effects* / Q000378:metabolism*; D030762:Estrous Cycle / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism*; D005260:Female; D007211:Indoles / Q000494:pharmacology; D019746:Intramolecular Oxidoreductases / Q000235:genetics / Q000378:metabolism; D008024:Ligands; D047492:Peroxisome Proliferator-Activated Receptors / Q000819:agonists / Q000378:metabolism*; D010642:Phenoxyacetates / Q000494:pharmacology; D011247:Pregnancy; D000071876:Prostaglandin-E Synthases; D011743:Pyrimidines / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics; D000077154:Rosiglitazone; D013552:Swine; D045162:Thiazolidinediones / Q000494:pharmacology; D002722:Chlorobenzenes
chemical_list: D015232:Dinoprostone; D007211:Indoles; D019746:Intramolecular Oxidoreductases; D008024:Ligands; D047492:Peroxisome Proliferator-Activated Receptors; D010642:Phenoxyacetates; D000071876:Prostaglandin-E Synthases; D011743:Pyrimidines; D012333:RNA, Messenger; D000077154:Rosiglitazone; D045162:Thiazolidinediones; C520164:4-(3-(2-propyl-3-hydroxy-4-acetyl)phenoxy)propyloxyphenoxy acetic acid; C060893:MK-886; D002722:Chlorobenzenes; C006253:pirinixic acid