title: Induction of mRNA for chemokines and chemokine receptors by prostaglandin F2α is dependent upon stage of the porcine corpus luteum and intraluteal progesterone.
abstract: This study tested the hypotheses that prostaglandin (PG) F(2α) increases expression of genes related to recruitment of leukocytes in mature but not early corpus luteum (CL) and that insensitivity to PGF(2α) action in early CL is dependent on high intraluteal progesterone (P4) concentrations. Experiment 1 examined early (0.5 h) and late (10 h) in vivo effects of PGF(2α) on mature (d 17 of pseudopregnancy) and early (d 9) porcine CL. Real-time PCR was used to measure mRNA for chemokines (IL8, CXCL2, CCL2, CCL8, CCL4, CCL11) and chemokine receptors (CCR1, CCR2, CXCR2, CCR5). Western blotting was used to measure protein expression and phosphorylation of nuclear factor-κB proteins. Treatment with PGF(2α) for 10 h increased mRNA for almost all of these genes (all expect CXCL2 and CCL11) in d 17 CL but not d 9 CL. Treatment with PGF(2α) also led to greater phosphorylation of nuclear factor-κB-1A protein in d 17 than d 9 CL. Experiment 2 had a 2 × 2 factorial design with d 9 gilts treated or not treated with epostane (3β-hydroxysteroid dehydrogenase inhibitor to suppress intraluteal P4) and treated or not treated with PGF(2α). Treatment with PGF(2α) (10 h) or epostane alone did not induce expression of any of these genes in d 9 CL. However, PGF(2α) + epostane increased expression of all of these genes except CCL11. In conclusion, PGF(2α) increases mRNA for chemokines and chemokine receptors in mature CL with similar PGF(2α) effects induced in early CL if intraluteal P4 is suppressed prior to PGF(2α) treatment.
authors.affiliation: Endocrinology-Reproductive Physiology Program and Department of Dairy Science, University of Wisconsin-Madison, 1675 Observatory Drive, Madison, Wisconsin 53706, USA.
authors.forename: Wenxiang
authors.initials: W
authors.lastname: Luo
authors.forename: Francisco J
authors.initials: FJ
authors.lastname: Diaz
authors.forename: Milo C
authors.initials: MC
authors.lastname: Wiltbank
mesh_terms: D015096:3-Hydroxysteroid Dehydrogenases / Q000037:antagonists & inhibitors; D000737:Androstenols / Q000494:pharmacology; D000818:Animals; D018925:Chemokines / Q000235:genetics / Q000378:metabolism*; D003338:Corpus Luteum / Q000378:metabolism*; D015237:Dinoprost / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D034461:Luteinization / Q000378:metabolism*; D016328:NF-kappa B / Q000378:metabolism; D010766:Phosphorylation; D011374:Progesterone / Q000378:metabolism*; D011499:Protein Processing, Post-Translational; D011555:Pseudopregnancy / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D019707:Receptors, Chemokine / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction; D034421:Sus scrofa; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D000737:Androstenols; D018925:Chemokines; D004791:Enzyme Inhibitors; D016328:NF-kappa B; D012333:RNA, Messenger; D019707:Receptors, Chemokine; D011374:Progesterone; C046855:epostane; D015237:Dinoprost; D015096:3-Hydroxysteroid Dehydrogenases