scholarly journals Ribonucleic Acid Binding Protein-Mediated Regulation of Luteinizing Hormone Receptor Expression in Granulosa Cells: Relationship to Sterol Metabolism

2007 ◽  
Vol 21 (9) ◽  
pp. 2233-2241 ◽  
Author(s):  
Lei Wang ◽  
Anil K. Nair ◽  
K. M. J. Menon
Keyword(s):  
Luteinizing Hormone ◽  
Granulosa Cells ◽  
Ribonucleic Acid ◽  
Hormone Receptor ◽  
Binding Protein ◽  
Receptor Expression ◽  
Luteinizing Hormone Receptor ◽  
Sterol Metabolism ◽  
Acid Binding Protein ◽  
Hormone Receptor Expression

scholarly journals The corticosterone-glucocorticoid receptor-AP1/CREB axis inhibits luteinizing hormone receptor expression in mouse granulosa cells

2020 ◽  
Author(s):  
Yinghui Wei ◽  
Ming Shen
Keyword(s):  
Luteinizing Hormone ◽  
Glucocorticoid Receptor ◽  
Granulosa Cells ◽  
Hormone Receptor ◽  
Follicular Development ◽  
The Body ◽  
Receptor Expression ◽  
Luteinizing Hormone Receptor ◽  
Control Group ◽  
Hormone Receptor Expression

Abstract Background 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 disorder of the body's endocrine system and damage to the body. Our previous work showed that corticosterone can block follicular development in mice. Since LH acts through binding with the LH receptor (LHR), the present study aimed to investigate whether and how CORT influence luteinizing hormone receptor expression in mouse ovarian granulosa cells (GCs). Methods For this purpose, 3-week-old ICR female mice were injected intraperitoneally with pregnant horse serum gonadotropin (PMSG). Meanwhile, the treatment group were injected with corticosterone corticosterone (1 mg/mouse) at intervals of 8 h; while the control group was injected with same volume of methyl sulfoxide (DMSO). Granulosa cells were collected at 24 h, 48 h, and 55 h after PMSG injection. For in vitro experiments, mice granulosa cells obtained from healthy follicles were treated with corticosterone alone, or together with inhibitors against glucocorticoid receptor (GR). Results The results showed that corticosterone caused down-regulation of luteinizing hormone receptor expression in granulosa cells, which was accompanied by impaired cell viability. Moreover, the effects of corticosterone was mediated by binding to its receptor in granulosa cells. Further investigations revealed that glucocorticoid receptor might regulated the transcription of luteinizing hormone receptor through inhibiting the expression of luteinizing hormone receptor transcription factors, including AP1 and CREB. Conclusions Our findings suggested a possible mechanism of corticosterone-induced anovulation involving the inhibition of luteinizing hormone receptor expression in granulosa cells by corticosterone-glucocorticoid receptor-AP1 / CREB axis.

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