Restraint stress and elevation of corticotrophin-releasing hormone in female mice impair oocyte competence through activation of the tumour necrosis factor α (TNF-α) system

Zhao, Xin-Yue; Li, Zhibin; Yuan, Haiqing; Han, Xianpei; Wu, Jia-Shun; Feng, Xiu-Yun; Zhang, Min; Tan, Jing-He

doi:10.1071/rd20002

Cited by 12 publications

(7 citation statements)

References 37 publications

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“…Song and colleagues [30] reported that CRH facilitated TNF-α production in CD14+ cells and triggered apoptosis in endothelial cells. Zhao et al [31] demonstrated that CRH enhanced TNF-α expression in ovarian cells. Thus, the present study provides evidence for the first time that CRH induces apoptosis of OECs by activating TNF-α signaling.…”

Section: Discussionmentioning

confidence: 99%

Corticosterone induced apoptosis of mouse oviduct epithelial cells independent of the TNF-α system

et al. 2021

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It has been reported in recent studies that restraint stress on pregnant mice during the preimplantation stage elevated corticotrophin-releasing hormone (CRH) and glucocorticoid levels in the serum and oviducts; furthermore, CRH and corticosterone (CORT) impacted preimplantation embryos indirectly by triggering the apoptosis of oviductal epithelial cells (OECs) through activation of the Fas system. However, it remains unclear whether TNF-α signaling is involved in CRH- and/or glucocorticoid-induced apoptosis of OECs. In the present study, it was shown that culture with either CRH or CORT induced significant apoptosis of OECs. The culture of OECs with CRH augmented both FasL expression and TNF-α expression. However, culture with CORT increased FasL, but decreased TNF-α, expression significantly. Although knocking down/knocking out FasL expression in OECs significantly ameliorated the proapoptotic effects of both CRH and CORT, knocking down/knocking out TNF-α expression relieved only the proapoptotic effect of CRH but not that of CORT. Taken together, our results demonstrated that CRH-induced OEC apoptosis involved both Fas signaling and TNF-α signaling. Conversely, CORT-induced OEC apoptosis involved only the Fas, but not the TNF-α, signaling pathway. The data obtained are crucial for our understanding of the mechanisms by which various categories of stress imposed on pregnant females impair embryo development, as well as for the development of measures to protect the embryo from the adverse effects of stress.

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Section: Discussionmentioning

confidence: 99%

Corticosterone induced apoptosis of mouse oviduct epithelial cells independent of the TNF-α system

et al. 2021

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“…Many papers have documented that CRH or cortisol trigger apoptosis in various somatic cells. For instance, CRH has been reported inducing apoptosis in neurons [ 32 ], in PC12 rat pheochromocytoma cell line [ 33 ], in microglial cells [ 34 ], in prostate cancer cell RM-1 [ 35 ] and in the mural granulosa cells (MGCs) of mouse ovarian follicles [ 36 , 37 ]. It is widely known that glucocorticoids can cause apoptosis in T lymphocytes [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

“…Song et al [ 48 ] reported that CRH promoted TNFα production by CD14+ cells. Zhao et al [ 37 ] observed that CRH treatment of mouse MGCs significantly increased their apoptotic percentages and levels of TNFα and TNFR1 expression, and in vitro knockdown by interfering RNA or in vivo knockout of the TNFα gene significantly alleviated the proapoptotic effect of CRH on MGCs.…”

Section: Discussionmentioning

confidence: 99%

Hypothalamic-Pituitary-Adrenal Hormones Impair Pig Fertilization and Preimplantation Embryo Development via Inducing Oviductal Epithelial Apoptosis: An In Vitro Study

Wang

et al. 2022

Cells

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Previous studies show that stressful events after ovulation in sows significantly impaired the embryo cleavage with a significant elevation of blood cortisol. However, the effects of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH) and cortisol on fertilization and embryo development remain to be specified, and whether they damage pig embryos directly or indirectly is unclear. This study demonstrated that embryo development was unaffected when pig parthenotes were cultured with different concentrations of CRH/ACTH/cortisol. However, embryo development was significantly impaired when the embryos were cocultured with pig oviductal epithelial cells (OECs) in the presence of CRH/cortisol or cultured in medium that was conditioned with CRH/cortisol-pretreated OECs (CRH/cortisol-CM). Fertilization in CRH/cortisol-CM significantly increased the rates of polyspermy. CRH and cortisol induced apoptosis of OECs through FAS and TNFα signaling. The apoptotic OECs produced less growth factors but more FASL and TNFα, which induced apoptosis in embryos. Pig embryos were not sensitive to CRH because they expressed no CRH receptor but the CRH-binding protein, and they were tolerant to cortisol because they expressed more 11-beta hydroxysteroid dehydrogenase 2 (HSD11B2) than HSD11B1. When used at a stress-induced physiological concentration, while culture with either CRH or cortisol alone showed no effect, culture with both significantly increased apoptosis in OECs. In conclusion, CRH and cortisol impair pig fertilization and preimplantation embryo development indirectly by inducing OEC apoptosis via the activation of the FAS and TNFα systems. ACTH did not show any detrimental effect on pig embryos, nor OECs.

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“…The duration of the procedure and the number of restriction episodes affect the intensity of the stress response and should be taken into account (Zhang et al, 2011;Wu X.F. et al, 2015;Zhao X.Y. et al, 2020).…”

Section: Modeling Psycho-emotional Stress In Laboratory Animalsmentioning

confidence: 99%

“…Besides, the addition of CRH to the culture medium during oocyte's in vitro maturation disrupted its development and increased the rate of apoptosis in granulosa cells (Liang et al, 2013). In another study, it was shown that a stressinduced increase of CRH both in blood and in the ovaries of female mice triggers apoptosis in oocytes and in ovarian granulosa cells due to the activation of the TNF-α system, which results in impaired oocyte competence (Zhao X.Y. et al, 2020).…”

Section: Influence Of Stress On the Reproductive Function Of Mammals:...mentioning

confidence: 99%

Psycho-emotional stress, folliculogenesis, and reproductive technologies: clinical and experimental data

et al. 2022

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Modern life, especially in large cities, exposes people to a high level of noise, high density of population, disrupted sleeping, large amount of excessive and controversial information as well as to other negative factors; all this may cause chronic psycho-emotional stress. The latest publications often use the term “Syndrome of megalopolis”, which means disruption of sleeping, high anxiety, and altered reproductive function. Medical treatment of infertility may also be considered as a stress factor, especially when infertility lasts for years and is aggravated with emotional frustration. Long-lasting distress may worsen health in general and suppress reproductive function, in particular. The review presents the data on the effects of maternal stress on folliculogenesis, especially when assisted reproductive technologies (ARTs) are used. Clinical data are presented alongside data from laboratory animal experiments. Different maternal stress models are taken into account in respect of their inf luence on oocyte maturation and embryo development. The interfering of psycho-emotional stress and reproductive function is the focus of the review. In these situations, exogenous hormones compensate for the stress-related disruption of the hypothalamic-pituitary-gonadal axis. When ARTs are implemented, stress-induced disruption of oogenesis is realized not via a decrease in hypothalamic and pituitary hormones, but by other ways, which involve paracrine mechanisms described in this review. Based on the literature analysis, one may conclude that stress negatively affects oocyte maturation in the ovary and suppresses subsequent embryo development. The role of some ovarian paracrine factors, such as BDNF, GDF-9, HB-EGF, TNF-α, and some others has been elucidated.

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Restraint stress and elevation of corticotrophin-releasing hormone in female mice impair oocyte competence through activation of the tumour necrosis factor α (TNF-α) system

Cited by 12 publications

References 37 publications

Corticosterone induced apoptosis of mouse oviduct epithelial cells independent of the TNF-α system

Corticosterone induced apoptosis of mouse oviduct epithelial cells independent of the TNF-α system

Hypothalamic-Pituitary-Adrenal Hormones Impair Pig Fertilization and Preimplantation Embryo Development via Inducing Oviductal Epithelial Apoptosis: An In Vitro Study

Psycho-emotional stress, folliculogenesis, and reproductive technologies: clinical and experimental data

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