Activation of Follicle-Stimulating Hormone Receptor in Adrenal Zona Fasciculata Cells Promotes Cortisol Secretion: Implications for the Development of Menopause-Associated Diseases

IF 1.6 4区 医学 Q4 ENDOCRINOLOGY & METABOLISM Experimental and Clinical Endocrinology & Diabetes Pub Date : 2024-09-16 DOI:10.1055/a-2376-5952
Jing-Gen Wu, Peng Zhao, Jing Yang, Ming-Juan Wang, Jian-Hua Chen, Xiao-Yong Li, Xue Ying, Yong-Chao Lu
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Abstract

Objective Changes in postmenopausal hormone levels are associated with a variety of disorders. This study elucidated the mechanism by which follicle-stimulating hormone (FSH) increases cortisol production involved in development of menopause-related diseases.

Methods The expression of FSH receptors (FSHRs) in murine adrenal zona fasciculata (AZF) cells and ATC7 cells was verified by immunofluorescence, western blotting and RT–PCR. The function of FSHR in promoting cortisol production was analyzed by cell culture and molecular biological methods. FSHR signaling pathways in ATC7 cells were analyzed by ELISA, qRT–PCR, and western blotting. Further, a mouse model was established by ovariectomy. Ovariectomized mice were treated with GnRHa. Ovariectomized mice initially received physiological doses of estrogen and were then injected with recombinant FSH. Then serum FSH, luteinizing hormone (LH), estradiol, and cortisol, and bone mineral density (BMD), blood pressure (BP) and heart rate (HR) were determined.

Results FSHRs were expressed in murine AZF cells and ATC7 cells. FSH accelerated cortisol production through activated protein kinase A (PKA), cyclic adenosine monophosphate (cAMP)-response element binding protein (CREB), protein kinase B (PKB/AKT) and 5ʼ AMP-activated protein kinase (MAPK) signaling pathways by Gsα-coupled FSHRs in ATC7 cells. Serum FSH levels (P<0.001) were elevated in ovariectomized mice with concurrent increases in cortisol (P<0.01), areal BMD (aBMD) (P<0.05), volumetric BMD (vBMD) (P<0.05), systolic BP (SBP) (P<0.05), diastolic BP (DBP) (P<0.05), and HR (P<0.05). However, the administration of GnRHa suppressed the increase in FSH levels and the elevation of cortisol, aBMD, vBMD, SBP, DBP, and HR induced by ovariectomy, even in the presence of normal serum estradiol levels.

Conclusion The study findings indicate that elevated FSH levels stimulate cortisol secretion, through a mechanism related to FSHRs expression in AZF cells.

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激活肾上腺筋膜细胞中的卵泡刺激素受体可促进皮质醇分泌:对更年期相关疾病发展的影响
目的 绝经后激素水平的变化与多种疾病有关。本研究阐明了卵泡刺激素(FSH)增加皮质醇分泌参与绝经相关疾病发生的机制。方法 通过免疫荧光、Western 印迹和 RT-PCR 验证 FSH 受体(FSHRs)在小鼠肾上腺筋膜带(AZF)细胞和 ATC7 细胞中的表达。通过细胞培养和分子生物学方法分析了FSHR促进皮质醇分泌的功能。通过ELISA、qRT-PCR和Western印迹法分析了ATC7细胞中的FSHR信号通路。此外,还通过卵巢切除术建立了小鼠模型。用GnRHa治疗切除卵巢的小鼠。卵巢切除的小鼠首先接受生理剂量的雌激素,然后注射重组 FSH。然后测定血清 FSH、黄体生成素(LH)、雌二醇和皮质醇,以及骨矿物质密度(BMD)、血压(BP)和心率(HR)。结果 FSHRs 在小鼠 AZF 细胞和 ATC7 细胞中表达。在ATC7细胞中,FSH通过Gsα耦合的FSHRs激活蛋白激酶A(PKA)、环磷酸腺苷(cAMP)-反应元件结合蛋白(CREB)、蛋白激酶B(PKB/AKT)和5ʼAMP-激活蛋白激酶(MAPK)信号通路加速皮质醇的产生。卵巢切除小鼠的血清 FSH 水平升高(P0.001),同时皮质醇(P0.01)、平均 BMD(aBMD)(P0.05)、容积 BMD(vBMD)(P0.05)、收缩压(SBP)(P0.05)、舒张压(DBP)(P0.05)和心率(P0.05)也升高。然而,即使在血清雌二醇水平正常的情况下,给予 GnRHa 也能抑制因卵巢切除而引起的 FSH 水平升高以及皮质醇、aBMD、vBMD、SBP、DBP 和 HR 的升高。结论 研究结果表明,FSH 水平升高会刺激皮质醇分泌,其机制与 AZF 细胞中 FSHRs 的表达有关。
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来源期刊
CiteScore
4.10
自引率
5.60%
发文量
72
审稿时长
3 months
期刊介绍: Publishing outstanding articles from all fields of endocrinology and diabetology, from molecular biology to clinical research, this journal is a brilliant resource. Since being published in English in 1983, the popularity of this journal has grown steadily, reflecting the importance of this publication within its field. Original contributions and short communications appear in each issue along with reviews addressing current topics. In addition, supplementary issues are published each year presenting abstracts or proceedings of national and international scientific meetings. The journal was initially published in German and is still the oldest endocrinological periodical in the German-language market!
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