» Articles » PMID: 27040909

Glucocorticoids Impair Oocyte Developmental Potential by Triggering Apoptosis of Ovarian Cells Via Activating the Fas System

Overview
Journal Sci Rep
Specialty Science
Date 2016 Apr 5
PMID 27040909
Citations 42
Authors
Affiliations
Soon will be listed here.
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.

Citing Articles

Impact of psychological stress on ovarian function: Insights, mechanisms and intervention strategies (Review).

Hu Y, Wang W, Ma W, Wang W, Ren W, Wang S Int J Mol Med. 2024; 55(2).

PMID: 39704226 PMC: 11670866. DOI: 10.3892/ijmm.2024.5475.


Maternal stress and the early embryonic microenvironment: investigating long-term cortisol effects on bovine oviductal epithelial cells using air-liquid interface culture.

Wahl F, Huo J, Du S, Schoen J, Chen S J Anim Sci Biotechnol. 2024; 15(1):129.

PMID: 39358766 PMC: 11447938. DOI: 10.1186/s40104-024-01087-4.


Premeiotic deletion of Eif2s2 causes oocyte arrest at the early diplotene stage and apoptosis in mice.

Zhou W, Li B, Wang Z, Liu S, Wang W, He S Cell Prolif. 2024; 57(12):e13718.

PMID: 39044637 PMC: 11628728. DOI: 10.1111/cpr.13718.


Role and action mechanisms of tPA in CRH-induced apoptosis of mouse oviductal epithelial and mural granulosa cells.

Yang Y, Zhang M, Hua Q, Ma R, Wang X, Yuan H J Reprod Dev. 2024; 70(4):238-246.

PMID: 38910127 PMC: 11310383. DOI: 10.1262/jrd.2024-028.


Association between depression and infertility risk among American women aged 18-45 years: the mediating effect of the NHHR.

Yang Q, Tao J, Xin X, Zhang J, Fan Z Lipids Health Dis. 2024; 23(1):178.

PMID: 38858764 PMC: 11163758. DOI: 10.1186/s12944-024-02164-3.


References
1.
Yazawa H, Sasagawa I, Nakada T . Apoptosis of testicular germ cells induced by exogenous glucocorticoid in rats. Hum Reprod. 2000; 15(9):1917-20. DOI: 10.1093/humrep/15.9.1917. View

2.
Kee B, Jung B, Lee S . A study on psychological strain in IVF patients. J Assist Reprod Genet. 2000; 17(8):445-8. PMC: 3455575. DOI: 10.1023/a:1009417302758. View

3.
de Los Santos M, Anderson D, Racowsky C, Hill J . Presence of Fas-Fas ligand system and bcl-2 gene products in cells and fluids from gonadotropin-stimulated human ovaries. Biol Reprod. 2000; 63(6):1811-6. DOI: 10.1095/biolreprod63.6.1811. View

4.
Waddell B, Hisheh S, Dharmarajan A, Burton P . Apoptosis in rat placenta is zone-dependent and stimulated by glucocorticoids. Biol Reprod. 2000; 63(6):1913-7. DOI: 10.1095/biolreprod63.6.1913. View

5.
Schmidt M, Lugering N, Lugering A, Pauels H, Schulze-Osthoff K, Domschke W . Role of the CD95/CD95 ligand system in glucocorticoid-induced monocyte apoptosis. J Immunol. 2001; 166(2):1344-51. DOI: 10.4049/jimmunol.166.2.1344. View