This study tested the hypotheses that prostaglandin (PG) F2α increases expression of genes related to recruitment of leukocytes in mature but not early corpus luteum (CL) and that insensitivity to PGF2α 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 PGF2α 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 PGF2α 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 PGF2α 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 PGF2α. Treatment with PGF2α (10 h) or epostane alone did not induce expression of any of these genes in d 9 CL. However, PGF2α + epostane increased expression of all of these genes except CCL11. In conclusion, PGF2α increases mRNA for chemokines and chemokine receptors in mature CL with similar PGF2α effects induced in early CL if intraluteal P4 is suppressed prior to PGF2α treatment
To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.