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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

作者: Li, Hui 1 ; Chang, Hsun-Ming 3 ; Li, Saijiao 2 ; Klausen, Christian 2 ; Shi, Zhendan 1 ; Leung, Peter C. K. 2 ;

作者机构: 1.Jiangsu Acad Agr Sci, Inst Anim Sci, Jiangsu Key Lab Food Qual & Safety, State Key Lab Cultivat Base,Minist Sci & Technol,K, Nanjing, Peoples R China

2.Univ British Columbia, BC Childrens Hosp, Dept Obstet & Gynaecol, Res Inst, Vancouver, BC, Canada

3.China Med Univ Hosp, Reprod Med Ctr, Dept Obstet & Gynecol, Taichung, Taiwan

4.Wuhan Univ, Reprod Med Ctr, Renmin Hosp, Wuhan, Peoples R China

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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