title: FAS/FASL-mediated cell death in the bovine endometrium.
abstract: In many mammals, endometrial cells are remodeled by apoptosis and cell proliferation throughout the estrous cycle. Although apoptosis is known to be induced by various factors involving two major apoptotic pathways (the death receptor- and mitochondria-mediated pathways), how it is regulated in the bovine endometrium is unclear. We examined (1) the cyclic expressions of apoptosis-related factors, FAS, DcR3, BCL2 and BAX, in the bovine endometrium and (2) the effect of death ligands on the viability of, and FAS mRNA expression in, cultured bovine endometrial epithelial and stromal cells. FAS expression did not change during the estrous cycle, whereas DcR3 expression was higher at the mid and late luteal stages than at the early luteal and follicular stages. BCL2 expression was higher at the late luteal stage than at the early luteal and follicular stages, and the BAX/BCL2 ratio was higher at the early luteal stage than at the late luteal stage. Treatment or pretreatment with tumor necrosis factor-α (TNF)+interferon γ (IFNG) in combination with FAS ligand significantly reduced the viability of both epithelial and stromal cells. Furthermore, TNF+IFNG treatment significantly increased the expression of FAS mRNA in both types of endometrial cells. The overall results suggest that both extrinsic and intrinsic pathways are involved in remodeling the bovine endometrium throughout the estrous cycle, and that the death ligands produced by immune cells and the endometrium play important roles in inducing cyclic endometrial cell death.
authors.affiliation: Laboratory of Reproductive Physiology, Graduate School of Natural Science and Technology, Okayama University, Okayama 700-8530, Japan.
authors.forename: Miki
authors.initials: M
authors.lastname: Arai
authors.affiliation: Laboratory of Reproductive Physiology, Graduate School of Natural Science and Technology, Okayama University, Okayama 700-8530, Japan.
authors.forename: Shin
authors.initials: S
authors.lastname: Yoshioka
authors.affiliation: Laboratory of Theriogenology, Joint Department of Veterinary Medicine, Faculty of Agriculture, Tottori University, Tottori 680-8550, Japan.
authors.forename: Ryo
authors.initials: R
authors.lastname: Nishimura
authors.affiliation: Laboratory of Reproductive Physiology, Graduate School of Natural Science and Technology, Okayama University, Okayama 700-8530, Japan. Electronic address: kokuda@cc.okayama-u.ac.jp.
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Okuda
mesh_terms: D000818:Animals; D002417:Cattle; D016923:Cell Death / Q000187:drug effects; D004717:Endometrium / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D004847:Epithelial Cells / Q000187:drug effects / Q000502:physiology; D030762:Estrous Cycle / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D053222:Fas Ligand Protein / Q000378:metabolism / Q000502:physiology*; D005260:Female; D007371:Interferon-gamma / Q000494:pharmacology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D053323:Receptors, Tumor Necrosis Factor, Member 6b / Q000235:genetics / Q000378:metabolism; D017154:Stromal Cells / Q000187:drug effects / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism; D019014:fas Receptor / Q000378:metabolism / Q000502:physiology*
chemical_list: D053222:Fas Ligand Protein; D019253:Proto-Oncogene Proteins c-bcl-2; D053323:Receptors, Tumor Necrosis Factor, Member 6b; D014409:Tumor Necrosis Factor-alpha; D051028:bcl-2-Associated X Protein; D019014:fas Receptor; D007371:Interferon-gamma
keywords: Apoptosis; Cattle; Endometrium; Remodeling