Characterization of the roles of amphiregulin and transforming growth factor beta 1 in microvasculature-like formation in human granulosa-lutein cells

文献类型： 外文期刊

第一作者： Li, Hui

作者： Li, Hui;Shi, Zhendan;Li, Hui;Li, Saijiao;Klausen, Christian;Leung, Peter C. K.;Chang, Hsun-Ming;Li, Saijiao

作者机构：

关键词： VE-cadherin; TGF-beta 1; amphiregulin; microvasculature-like formation; human granulosa cells

期刊名称：FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY （ 影响因子：6.081； 五年影响因子：6.576 ）

ISSN： 2296-634X

年卷期： 2022 年 10 卷

页码：

收录情况： SCI

摘要： Vascular endothelial-cadherin (VE-cadherin) is an essential component that regulates angiogenesis during corpus luteum formation. Amphiregulin (AREG) and transforming growth factor beta 1 (TGF-beta 1) are two intrafollicular factors that possess opposite functions in directing corpus luteum development and progesterone synthesis in human granulosa-lutein (hGL) cells. However, whether AREG or TGF-beta 1 regulates the VE-cadherin expression and subsequent angiogenesis in the human corpus luteum remains to be elucidated. Results showed that hGL cells cultured on Matrigel spontaneously formed capillary-like and sprout-like microvascular networks. Results of specific inhibitor treatment and small interfering RNA-mediated knockdown revealed that AREG promoteed microvascular-like formation in hGL cells by upregulating the VE-cadherin expression mediated by the epidermal growth factor receptor (EGFR)-extracellular signal-regulated kinase1/2 (ERK1/2) signaling pathway. However, TGF-beta 1 suppressed microvascular-like formation in hGL cells by downregulating VE-cadherin expression mediated by the activin receptor-like kinase (ALK)5-Sma- and Mad-related protein (SMAD)2/3/4 signaling pathway. Collectively, this study provides important insights into the underlying molecular mechanisms by which TGF-beta 1 and AREG differentially regulate corpus luteum formation in human ovaries.

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