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Corticosterone induced apoptosis of mouse oviduct epithelial cells independent of the TNF-α system
Journal of Reproduction and Development ( IF 1.8 ) Pub Date : 2021-01-01 , DOI: 10.1262/jrd.2020-122
Ying-Qi Zhao 1 , Ren-Ren Chen 1 , Qiao-Qiao Kong 1 , Jin-Song An 1 , Xin-Yue Zhao 1 , Shuai Gong 1 , Hong-Jie Yuan 1 , Jing-He Tan 1
Affiliation  

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.

中文翻译:

皮质酮诱导小鼠输卵管上皮细胞凋亡,不依赖于 TNF-α 系统

最近的研究表明,在胚胎植入前阶段对怀孕小鼠施加压力会升高血清和输卵管中的促肾上腺皮质激素释放激素 (CRH) 和糖皮质激素水平;此外,CRH 和皮质酮 (CORT) 通过激活 Fas 系统触发输卵管上皮细胞 (OEC) 的凋亡,从而间接影响植入前胚胎。然而,尚不清楚 TNF-α 信号是否参与 CRH 和/或糖皮质激素诱导的 OEC 细胞凋亡。在本研究中,显示了具有 CRH 或 CORT 的培养物诱导了 OEC 的显着凋亡。OECs 与 CRH 的培养增强了 FasL 表达和 TNF-α 表达。然而,CORT 培养增加了 FasL,但显着降低了 TNF-α 的表达。尽管敲除/敲除 OEC 中 FasL 的表达显着改善了 CRH 和 CORT 的促凋亡作用,但敲除/敲除 TNF-α 表达仅缓解了 CRH 的促凋亡作用,而不能缓解 CORT 的促凋亡作用。总之,我们的结果表明 CRH 诱导的 OEC 细胞凋亡涉及 Fas 信号和 TNF-α 信号。相反,CORT 诱导的 OEC 细胞凋亡仅涉及 Fas,而不涉及 TNF-α 信号通路。获得的数据对于我们了解施加给怀孕女性的各种压力损害胚胎发育的机制以及制定保护胚胎免受压力不利影响的措施至关重要。敲低/敲除 TNF-α 表达仅减轻 CRH 的促凋亡作用,而不能减轻 CORT 的促凋亡作用。总之,我们的结果表明 CRH 诱导的 OEC 细胞凋亡涉及 Fas 信号和 TNF-α 信号。相反,CORT 诱导的 OEC 细胞凋亡仅涉及 Fas,而不涉及 TNF-α 信号通路。获得的数据对于我们了解施加给怀孕女性的各种压力损害胚胎发育的机制以及制定保护胚胎免受压力不利影响的措施至关重要。敲低/敲除 TNF-α 表达仅减轻 CRH 的促凋亡作用,而不能减轻 CORT 的促凋亡作用。总之,我们的结果表明 CRH 诱导的 OEC 细胞凋亡涉及 Fas 信号和 TNF-α 信号。相反,CORT 诱导的 OEC 细胞凋亡仅涉及 Fas,而不涉及 TNF-α 信号通路。获得的数据对于我们了解施加给怀孕女性的各种压力损害胚胎发育的机制以及制定保护胚胎免受压力不利影响的措施至关重要。信号通路。获得的数据对于我们了解施加给怀孕女性的各种压力损害胚胎发育的机制以及制定保护胚胎免受压力不利影响的措施至关重要。信号通路。获得的数据对于我们了解施加给怀孕女性的各种压力损害胚胎发育的机制以及制定保护胚胎免受压力不利影响的措施至关重要。
更新日期:2021-01-01
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