title: Acquisition of luteolytic capacity: changes in prostaglandin F2alpha regulation of steroid hormone receptors and estradiol biosynthesis in pig corpora lutea.
abstract: The pig corpora lutea (CL) acquires luteolytic capacity at about Day 13 of the estrous cycle, after which luteolysis occurs in response to prostaglandin F2alpha (PGF2alpha) treatment. We postulated that differences in transcription factors such as the steroid hormone receptors may be responsible for the differences in PGF2alpha-induced gene expression after acquisition of luteolytic capacity. In these studies, we evaluated the effect of PGF2alpha on luteal expression of receptors for progesterone (nuclear and membrane progesterone receptor [PR]), estradiol (ERalpha and ERbeta), glucocorticoid, androgens, and two enzymes in estradiol synthesis (P450-17alpha and aromatase). Two experiments were conducted to examine the early (0.5 h, experiment I) and late (10 h, experiment II) effects of PGF(2alpha) on the expression of these receptors in CL with (Day 17) or without (Day 9) luteolytic capacity. PGF2alpha decreased ERalpha mRNA (35%) and increased ERbeta mRNA (558%) and protein (376%) only in Day 17 CL and not Day 9. The estradiol biosynthetic pathway was upregulated by PGF2alpha in Day 17 CL but not Day 9 CL, with a dramatic increase in aromatase mRNA and luteal estradiol content. Nuclear PR was not affected by PGF2alpha, but was greater (176%) in Day 9 CL, while a putative membrane PR was greater (156%) in Day 17 than Day 9 CL. There were no detectable changes in glucocorticoid or androgen receptor mRNA. Thus, luteolytic capacity is associated with upregulation of estradiol biosynthesis, which in conjunction with increased ERbeta expression and altered PR expression may promote luteolysis in the pig CL.
authors.affiliation: Endocrinology-Reproductive Physiology Program and Department of Dairy Science, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA.
authors.forename: Francisco J
authors.initials: FJ
authors.lastname: Diaz
authors.forename: Milo C
authors.initials: MC
authors.lastname: Wiltbank
mesh_terms: D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D003338:Corpus Luteum / Q000187:drug effects* / Q000502:physiology*; D015237:Dinoprost / Q000494:pharmacology*; D004958:Estradiol / Q000096:biosynthesis*; D047628:Estrogen Receptor alpha / Q000378:metabolism; D047629:Estrogen Receptor beta / Q000378:metabolism; D005260:Female; D003341:Luteolysis / Q000502:physiology*; D011944:Receptors, Androgen / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000378:metabolism*; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D013552:Swine
chemical_list: D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D011944:Receptors, Androgen; D011956:Receptors, Cell Surface; D018160:Receptors, Cytoplasmic and Nuclear; D011965:Receptors, Glucocorticoid; D011980:Receptors, Progesterone; D004958:Estradiol; D015237:Dinoprost