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The Corticosterone-Glucocorticoid Receptor-AP1/CREB Axis Inhibits the Luteinizing Hormone Receptor Expression in Mouse Granulosa Cells

文献类型： 外文期刊

作者： Zhang, Xuan 1 ; Wei, Yinghui 1 ; Li, Xiaoxuan 1 ; Li, Chengyu 1 ; Zhang, Liangliang 1 ; Liu, Zhaojun 1 ; Cao, Yan 1 ; Li, Weijian 1 ; Zhang, Xiying 1 ; Zhang, Jiaqing 3 ; Shen, Ming 1 ; Liu, Honglin 1 ;

作者机构： 1.Nanjing Agr Univ, Coll Anim Sci & Technol, Nanjing 210095, Peoples R China

2.Hangzhou Acad Agr Sci, Hangzhou 310024, Peoples R China

3.Henan Acad Agr Sci, Inst Anim Husb & Vet Sci, Zhengzhou 450002, Peoples R China

关键词： corticosterone; granulosa cells; luteinizing hormone receptor; glucocorticoid receptor

期刊名称：INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES （ 影响因子：6.208； 五年影响因子：6.628 ）

ISSN：

年卷期： 2022 年 23 卷 20 期

页码：

收录情况： SCI

摘要： Under stress conditions, luteinizing hormone (LH)-mediated ovulation is inhibited, resulting in insufficient oocyte production and excretion during follicular development. When the body is stressed, a large amount of corticosterone (CORT) is generated, which will lead to a disorder of the body's endocrine system and damage to the body. Our previous work showed that CORT can block follicular development in mice. Since LH acts through binding with the luteinizing hormone receptor (Lhcgr), the present study aimed to investigate whether and how corticosterone (CORT) influences Lhcgr expression in mouse ovarian granulosa cells (GCs). For this purpose, three-week-old ICR female mice were injected intraperitoneally with pregnant mare serum gonadotropin (PMSG). In addition, the treatment group was injected with CORT (1 mg/mouse) at intervals of 8 h and the control group was injected with the same volume of methyl sulfoxide (DMSO). GCs were collected at 24 h, 48 h, and 55 h after PMSG injection. For in vitro experiments, the mouse GCs obtained from healthy follicles were treated with CORT alone, or together with inhibitors against the glucocorticoid receptor (Nr3c1). The results showed that the CORT caused a downregulation of Lhcgr expression in GCs, which was accompanied by impaired cell viability. Moreover, the effect of the CORT was mediated by binding to its receptor (Nr3c1) in GCs. Further investigation revealed that Nr3c1 might regulate the transcription of Lhcgr through inhibiting the expression of Lhcgr transcription factors, including AP1 and Creb. Taken together, our findings suggested a possible mechanism of CORT-induced anovulation involving the inhibition of Lhcgr expression in GCs by the CORT-Nr3c1-AP1/Creb axis.

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