title: Cortisol is a suppressor of apoptosis in bovine corpus luteum.
abstract: Glucocorticoid (GC) acts as a modulator of physiological functions in several organs. In the present study, we examined whether GC suppresses luteolysis in bovine corpus luteum (CL). Cortisol (an active GC) reduced the mRNA expression of caspase 8 (CASP8) and caspase 3 (CASP3) and reduced the enzymatic activity of CASP3 and cell death induced by tumor necrosis factor (TNF) and interferon gamma (IFNG) in cultured bovine luteal cells. mRNAs and proteins of GC receptor (NR3C1), 11beta-hydroxysteroid dehydrogenase type 1 (HSD11B1), and HSD11B2 were expressed in CL throughout the estrous cycle. Moreover, the protein expression and the enzymatic activity of HSD11B1 were high at the early and the midluteal stages compared to the regressed luteal stage. These results suggest that cortisol suppresses TNF-IFNG-induced apoptosis in vitro by reducing apoptosis signals via CASP8 and CASP3 in bovine CL and that the local increase in cortisol production resulting from increased HSD11B1 at the early and midluteal stages helps to maintain CL function by suppressing apoptosis of luteal cells.
authors.affiliation: Laboratory of Reproductive Endocrinology, Graduate School of Natural Science and Technology, Okayama University, Okayama 700-8530, Japan.
authors.forename: Junichi
authors.initials: J
authors.lastname: Komiyama
authors.forename: Ryo
authors.initials: R
authors.lastname: Nishimura
authors.forename: Hwa-Yong
authors.initials: HY
authors.lastname: Lee
authors.forename: Ryosuke
authors.initials: R
authors.lastname: Sakumoto
authors.forename: Masafumi
authors.initials: M
authors.lastname: Tetsuka
authors.forename: Tomas J
authors.initials: TJ
authors.lastname: Acosta
authors.forename: Dariusz J
authors.initials: DJ
authors.lastname: Skarzynski
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Okuda
mesh_terms: D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1 / Q000378:metabolism; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2 / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D053148:Caspase 3 / Q000378:metabolism; D053181:Caspase 8 / Q000378:metabolism; D002417:Cattle; D002478:Cells, Cultured; D003338:Corpus Luteum / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D053222:Fas Ligand Protein / Q000378:metabolism; D005260:Female; D006854:Hydrocortisone / Q000494:pharmacology / Q000502:physiology*; D007371:Interferon-gamma / Q000494:pharmacology; D008184:Luteal Cells / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D053222:Fas Ligand Protein; D012333:RNA, Messenger; D011965:Receptors, Glucocorticoid; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2; D053148:Caspase 3; D053181:Caspase 8; D006854:Hydrocortisone