title: Glucocorticoids impair oocyte developmental potential by triggering apoptosis of ovarian cells via activating the Fas system.
abstract: Previous studies indicate that stress damages oocytes with increased secretion of glucorticoids. However, although injection of female mice with cortisol decreased oocyte competence, exposure of mouse oocytes directly to physiological or stress-induced concentrations of glucorticoids did not affect oocyte maturation and embryo development. This study has explored the mechanisms by which glucocorticoids impair oocyte competence. Female mice were injected with cortisol and the effects of cortisol-injection on oocyte competence, ovarian cell apoptosis and Fas/FasL activation were observed. The results showed that cortisol-injection decreased (a) oocyte developmental potential, (b) the E2/P4 ratio in serum and ovaries, and (c) expression of insulin-like growth factor 1, brain-derived neurotrophic factor and glucocorticoid receptor in mural granulosa cells (MGCs), while increasing levels of (a) cortisol in serum and ovaries, (b) apoptosis in MGCs and cumulus cells (CCs), (c) FasL secretion in ovaries and during oocyte maturation in vitro, and (d) Fas in MGCs, CCs and oocytes. The detrimental effects of cortisol-injection on oocyte competence and apoptosis of MGCs and CCs were significantly relieved when the gld (generalized lymphoproliferative disorder) mice harboring FasL mutations were observed. Together, the results suggested that glucocorticoids impair oocyte competence by triggering apoptosis of ovarian cells via activating the Fas system.
authors.affiliation: College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City 271018, P. R. China.
authors.forename: Hong-Jie
authors.initials: HJ
authors.lastname: Yuan
authors.affiliation: College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City 271018, P. R. China.
authors.forename: Xiao
authors.initials: X
authors.lastname: Han
authors.affiliation: College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City 271018, P. R. China.
authors.forename: Nan
authors.initials: N
authors.lastname: He
authors.affiliation: College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City 271018, P. R. China.
authors.forename: Guo-Liang
authors.initials: GL
authors.lastname: Wang
authors.affiliation: College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City 271018, P. R. China.
authors.forename: Shuai
authors.initials: S
authors.lastname: Gong
authors.affiliation: College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City 271018, P. R. China.
authors.forename: Juan
authors.initials: J
authors.lastname: Lin
authors.affiliation: College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City 271018, P. R. China.
authors.forename: Min
authors.initials: M
authors.lastname: Gao
authors.affiliation: College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai-an City 271018, P. R. China.
authors.forename: Jing-He
authors.initials: JH
authors.lastname: Tan
mesh_terms: D000818:Animals; D017209:Apoptosis; D053222:Fas Ligand Protein / Q000378:metabolism*; D005260:Female; D018507:Gene Expression Regulation, Developmental; D006107:Granulosa Cells / Q000187:drug effects / Q000378:metabolism; D006854:Hydrocortisone / Q000008:administration & dosage* / Q000494:pharmacology; D051379:Mice; D009865:Oocytes / Q000166:cytology* / Q000187:drug effects; D009866:Oogenesis / Q000187:drug effects*; D019014:fas Receptor / Q000378:metabolism*
chemical_list: D053222:Fas Ligand Protein; C491899:Fas protein, mouse; C505658:Fasl protein, mouse; D019014:fas Receptor; D006854:Hydrocortisone