Glucocorticoid influence on porcine granulosa cell IGF-I and steroid hormone production in vitro

Viveiros, M.M.; Liptrap, R.M.

doi:10.1016/s0093-691x(99)80009-0

Cited by 16 publications

(4 citation statements)

References 37 publications

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“…Using cultures of rat osteoblasts, Delany and Canalis 44 demonstrated that cortisol decreased Igf1 mRNA by approximately 50% through decreasing gene transcription. Furthermore, studies in the pig have shown that increased glucorticoid concentrations can disrupt ovarian IGF1 synthesis and IGF action both in vitro 45 and in vivo 46 . In rats, both acute and chronic corticosterone administration significantly decreased Bdnf mRNA and protein in the hippocampus 47 48 .…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids impair oocyte developmental potential by triggering apoptosis of ovarian cells via activating the Fas system

Yuan

Han

et al. 2016

Sci Rep

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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.

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Section: Discussionmentioning

confidence: 99%

Glucocorticoids impair oocyte developmental potential by triggering apoptosis of ovarian cells via activating the Fas system

Yuan

Han

et al. 2016

Sci Rep

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“…Glucocorticoids were found to enhance FSH-stimulated progesterone synthesis in cultured granulosa cells of rats and cattle [77][78][79] and to suppress P450 aromatase activity and decrease the number of LH receptors in rats [78,80], cattle [79], and pigs [81]. Furthermore, porcine studies have demonstrated that increased glucocorticoid concentrations can disrupt ovarian IGF1 synthesis and IGF action both in vitro and in vivo [82,83]. On the other hand, glucocorticoids were found to promote androgen production by cultured thecal cells in cattle [84].…”

Section: Liang Et Almentioning

confidence: 99%

Restraint Stress Impairs Oocyte Developmental Potential in Mice: Role of CRH-Induced Apoptosis of Ovarian Cells1

Liang

Wei

Cheng

et al. 2013

Biology of Reproduction

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This study examined the role of CRH-induced ovarian cell apoptosis in the restraint stress (RS)-induced impairment of oocyte competence. Oocyte percentages of apoptotic cumulus cells (CCs) did not differ between stressed and control mice before in vitro maturation (IVM) but became significantly higher in stressed mice after IVM without serum, growth factor, and hormone. The level of Bcl2 mRNA decreased significantly in mural granulosa cells (MGCs) and ovarian homogenates after RS. Whereas ovarian estradiol, testosterone, and IGF1 decreased, cortisol and progesterone increased significantly following RS. RS increased the level of CRH in serum, ovary, and oocyte while enhancing the expression of CRHR1 in CCs, MGCs, and thecal cells. RS down-regulated ovarian expression of glucocorticoid receptor and brain-derived neurotrophic factor. Furthermore, CRH supplementation to IVM medium impaired oocyte developmental potential while increasing apoptotic CCs, an effect that was completely overcome by addition of the CRHR1 antagonist antalarmin. Results suggest that RS impaired oocyte competence by increasing CRH but not glucocorticoids. Increased CRH initiated a latent apoptotic program in CCs and oocytes during their intraovarian development, which was executed later during IVM to impair oocyte competence. Thus, elevated CRH interacted with increased CRHR1 on thecal cells and MGCs, reducing the production of testosterone, estrogen, and IGF1 while increasing the level of progesterone. The imbalance between estrogen and progesterone and the decreased availability of growth factors triggered apoptosis of MGCs and facilitated CC expression of CRHR1, which interacted with the oocyte-derived CRH later during IVM to induce CC apoptosis and reduce oocyte competence.

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“…However, the interaction between these two steroids during luteinization is not yet fully understood. For instance, cortisol may promote luteinization, as glucocorticoids have been shown to increase P4 production in cultured GCs from various species, including cattle [14][15][16][17][18][19][20][21]. P4 may stimulate cortisol production, as we previously found that P4 upregulates HSD11B1 expression and the conversion of cortisone to cortisol in the maturing cumulus oophorus [22].…”

Section: Introductionmentioning

confidence: 81%

Progesterone modulates HSD11B1-mediated cortisol production in luteinized bovine granulosa cells

Mukangwa

Tetsuka

2023

Journal of Reproduction and Development

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Progesterone (P4) and cortisol production increase in luteinized granulosa cells (LGCs) during the periovulatory period, but their interaction is not well established. Therefore, we investigated their interaction in cultured bovine LGCs. Granulosa cells were collected from follicles of 2-5 mm in diameter and cultured in DMEM/F-12 supplemented with 10% fetal calf serum for up to 14 days. P4 production and the expression of steroidogenic acute regulatory protein (STAR), cholesterol side-chain cleavage enzyme (CYP11A1), and 3β-hydroxysteroid dehydrogenase type 1 (HSD3B1) rapidly increased until day 10 and remained high thereafter. No de novo of cortisol from P4 was detected during the culture period.The expression of 11β-hydroxysteroid dehydrogenase type 1 (HSD11B1), which converts cortisone to cortisol, increased dramatically on day two, decreased until day 8, and remained relatively constant. To investigate how P4 and cortisol influence each other's production, LGCs were treated with trilostane (a P4 synthesis inhibitor), nomegestrol acetate (NA, a synthetic progestogen), P4, and/or cortisol for 24 h on days 6 and 12 of culture. Trilostane suppressed P4 and STAR expression while elevating HSD11B1 and HSD3B1 expression and cortisol production. Concomitant treatment with NA or P4 dose-dependently decreased cortisol production and HSD11B1 and HSD3B1 expression but elevated STAR expression in both days 6 and 12. Conversely, cortisol treatment increased HSD11B1 and HSD3B1 expression and decreased STAR expression without influencing P4 production. These results indicate that progestogens suppress cortisol production by modulating HSD11B1 expression and that progestogens and cortisol differentially regulate STAR, HSD3B1, and HSD11B1 expression in bovine LGCs.

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Glucocorticoid influence on porcine granulosa cell IGF-I and steroid hormone production in vitro

Cited by 16 publications

References 37 publications

Glucocorticoids impair oocyte developmental potential by triggering apoptosis of ovarian cells via activating the Fas system

Glucocorticoids impair oocyte developmental potential by triggering apoptosis of ovarian cells via activating the Fas system

Restraint Stress Impairs Oocyte Developmental Potential in Mice: Role of CRH-Induced Apoptosis of Ovarian Cells1

Progesterone modulates HSD11B1-mediated cortisol production in luteinized bovine granulosa cells

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