title: Role of cell death ligand and receptor system on regulation of follicular atresia in pig ovaries.
abstract: Several hundred thousand primordial follicles are present in the mammalian ovary, however, only a limited number develop to the pre-ovulatory stage, and then finally ovulate. The others, more than 99%, will be eliminated through a degenerative process called 'atresia'. The endocrinological regulatory mechanisms involved in follicular development and atresia have been characterized to a large extent, but the precise temporal and molecular mechanisms involved in the regulation of these events have remained unknown. From many recent studies, it is suggested that the apoptosis in ovarian granulosa cells plays a crucial role in follicular atresia. Notably, death ligand-receptor interaction and subsequent intracellular signalling have been demonstrated to be the key mechanisms regulating granulosa cell apoptosis. In this review, we provide an overview of granulosa cell apoptosis regulated by death ligand-receptor signalling. The roles of death ligands and receptors [Fas ligand (FasL)-Fas, tumour necrosis factor (TNF)alpha-TNF receptor (TNFR), and TNFalpha-related apoptosis-inducing ligand (TRAIL)-TRAIL receptor (TRAILR)] and intracellular death-signal mediators [Fas-associated death domain protein (FADD), TNF receptor 1-associated death domain protein (TRADD), caspases, apoptotic protease-activating factor 1 (Apaf1), TNFR-associated factor 2 (TRAF2), and cellular FLICE-like inhibitory protein (cFLIP), etc.] in granulosa cells will be discussed.
authors.affiliation: Animal Resource Science Center, University of Tokyo, Kasama, Japan. amanabe@mail.ecc.u-tokyo.ac.jp
authors.forename: N
authors.initials: N
authors.lastname: Manabe
authors.forename: F
authors.initials: F
authors.lastname: Matsuda-Minehata
authors.forename: Y
authors.initials: Y
authors.lastname: Goto
authors.forename: A
authors.initials: A
authors.lastname: Maeda
authors.forename: Y
authors.initials: Y
authors.lastname: Cheng
authors.forename: S
authors.initials: S
authors.lastname: Nakagawa
authors.forename: N
authors.initials: N
authors.lastname: Inoue
authors.forename: K
authors.initials: K
authors.lastname: Wongpanit
authors.forename: H
authors.initials: H
authors.lastname: Jin
authors.forename: H
authors.initials: H
authors.lastname: Gonda
authors.forename: J
authors.initials: J
authors.lastname: Li
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism*; D053446:CASP8 and FADD-Like Apoptosis Regulating Protein / Q000378:metabolism; D053222:Fas Ligand Protein / Q000378:metabolism; D053200:Fas-Associated Death Domain Protein / Q000378:metabolism; D005260:Female; D005496:Follicular Atresia / Q000502:physiology*; D006107:Granulosa Cells / Q000166:cytology / Q000502:physiology*; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism; D006080:Ovarian Follicle; D053218:Receptors, Death Domain / Q000502:physiology; D013552:Swine; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism / Q000502:physiology
chemical_list: D051017:Apoptosis Regulatory Proteins; D053446:CASP8 and FADD-Like Apoptosis Regulating Protein; D053222:Fas Ligand Protein; D053200:Fas-Associated Death Domain Protein; D047908:Intracellular Signaling Peptides and Proteins; D053218:Receptors, Death Domain; D053221:TNF-Related Apoptosis-Inducing Ligand; D014409:Tumor Necrosis Factor-alpha