title: Auto-amplification system for prostaglandin F2α in bovine corpus luteum.
abstract: The bovine corpus luteum (CL) is hypothesized to utilize a local auto-amplification system for prostaglandin (PG) F2α production. The objective of the present study was to determine if such a PGF2α auto-amplification system exists in the bovine CL, and if so, which factors regulate it. PGF2α significantly stimulated intra-luteal PGF2α production in all luteal phases, but did not affect PGE2 production. The stimulatory effect of exogenous PGF2α on CL PGF2α production was lower at the early luteal phase. Indomethacin, an inhibitor of prostaglandin-endoperoxide synthase (PTGS), significantly suppressed the PGF2α-stimulated PGF2α production by luteal tissue, indicating that the PGF2α in the medium was of luteal origin. Consistent with these secreted-PGF2α profiles, PGF2α receptor (PTGFR) protein expression was higher during the mid and late luteal phases than at early and developing luteal phases. Treatment of cultured bovine luteal cells obtained from the mid-luteal phase with PGF2α (1 µM) significantly increased the expressions of PTGS2, PGF synthase (PGFS), and carbonyl reductase1 (CBR1) at 24 hr post-treatment. Together, these results suggest the presence of a local auto-amplification system for PGF2α mediated by PTGS2, PGFS, and CBR1 in the bovine CL, which may play an important role in luteolysis.
authors.affiliation: Graduate School of Natural Science and Technology, Okayama University, Okayama, Japan.
authors.forename: Asuka
authors.initials: A
authors.lastname: Kumagai
authors.forename: Shin
authors.initials: S
authors.lastname: Yoshioka
authors.forename: Ryosuke
authors.initials: R
authors.lastname: Sakumoto
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Okuda
mesh_terms: D000818:Animals; D002417:Cattle; D002478:Cells, Cultured; D003338:Corpus Luteum / Q000378:metabolism*; D015237:Dinoprost / Q000032:analysis / Q000378:metabolism* / Q000502:physiology*; D015232:Dinoprostone / Q000032:analysis / Q000378:metabolism; D004958:Estradiol / Q000032:analysis / Q000378:metabolism; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D008183:Luteal Phase / Q000378:metabolism; D011374:Progesterone / Q000032:analysis / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*
chemical_list: D011374:Progesterone; D004958:Estradiol; D015237:Dinoprost; D015232:Dinoprostone; D007213:Indomethacin