IMR Press / FBE / Volume 3 / Issue 4 / DOI: 10.2741/E342

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Interactions of thyroid hormone and FSH in the regulation of rat granulosa cell apoptosis
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1 State Key Laboratory for Agro-Biotechnology, College of Biological Science, China Agricultural University, Beijing 100193, Peoples’ Republic of China
2 Reproductive Biology Unit, Departments of Cellular and Molecular Medicine, and Obstetrics & Gynaecology, University of Ottawa, Ottawa, Ontario, Canada K1Y 4E9
3 Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada
4 World Class University (WCU) Biomodulation Major, Department of Agricultural Biotechnology, College of Agriculture and Life Sciences, Seoul National University, Seoul 151-921, Republic of Korea

*Author to whom correspondence should be addressed.

Front. Biosci. (Elite Ed) 2011, 3(4), 1401–1413; https://doi.org/10.2741/E342
Published: 1 June 2011
Abstract

Thyroid hormone (TH) is important for normal reproductive function. Our previous studies indicate that FSH increases preantral follicle growth in vitro, a response markedly enhanced by triiodothyronine (T3). However, the nature of this hormonal interaction is poorly understood. The objective of this study was to determine if and how T3 modulate FSH-induced expression and actions of granulosa cell intracellular survival and death intermediates. We investigated the possible involvement of Src and PI3K/Akt pathway in the regulation of granulosa cell survival. We demonstrated that, while ineffective alone (0.1-100 nM), T3 markedly enhanced FSH (100 ng/ml)-induced granulosa cell phospho-Src and phospho-Akt contents and Xiap expression in vitro. The effects of T3 were concentration-dependent, with maximal responses at 1.0 nM. FSH alone decreased Fas Ligand (FasL) content irrespective of the presence of T3. Co-treatment of cell with T3 and FSH decreased Fas content, although neither hormone alone elicited a significant response. Taken together, the present study demonstrates that T3 potentiates the cell survival action of FSH through Src- and PI3K-mediated Xiap up-regulation and decreased Fas and FasL expression.

Keywords
thyroid hormone
FSH
granulosa cell
apoptosis
Xiap
Fas
Fas ligand
Src.
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