Department of Clinical laboratory, Qianjiang Hospital of Yangtze University, Qianjiang, 433100, Hubei, China.
College of Mechanical Engineering, Dongguan University of Technology, Dongguan, 523808, Guangdong, China.
Gene Ther. 2021 Apr;28(3-4):155-161. doi: 10.1038/s41434-020-00195-w. Epub 2020 Sep 29.
Follicle-stimulating hormone (FSH) is a pituitary glycoprotein that regulates follicle maturation through its binding to follicle-stimulating hormone receptor (FSHR). Endothelial cells express FSHR, but its exact role in endothelial cells remains unclear. Here we show that FSHR expression was detectable in human umbilical vein endothelial cells (HUVECs). FSH stimulation promoted HUVECs migration but not proliferation. Because FSHR is a GPCR, FSH treatment triggers the activation of cAMP-PKA signaling pathways, and the JAK-STAT, PI3K-AKT, and JNK-MAPK pathways. RNAi of FSHR dramatically attenuated the activation effect of FSH on HUVECs migration, as well as the related signaling pathways. Treatment of FSH in HUVECs also transcriptionally upregulated the expression of VAV3 and LAMA2, suppression either of VAV3 or LAMA2 by RNAi attenuated the FSH's effect on HUVECs migration. All of these results indicated a functional role of FSH in the regulation of endothelial cells.
卵泡刺激素（FSH）是一种垂体糖蛋白，通过与卵泡刺激素受体（FSHR）结合来调节卵泡成熟。内皮细胞表达 FSHR，但它在内皮细胞中的确切作用尚不清楚。在这里，我们显示 FSHR 表达可检测到人脐静脉内皮细胞（HUVECs）中。FSH 刺激促进 HUVECs 迁移，但不促进增殖。由于 FSHR 是一种 G 蛋白偶联受体（GPCR），FSH 处理会触发 cAMP-PKA 信号通路以及 JAK-STAT、PI3K-AKT 和 JNK-MAPK 通路的激活。FSHR 的 RNAi 显著减弱了 FSH 对 HUVECs 迁移的激活作用，以及相关的信号通路。在 HUVECs 中用 FSH 处理也可转录地上调 VAV3 和 LAMA2 的表达，用 RNAi 抑制 VAV3 或 LAMA2 均可减弱 FSH 对 HUVECs 迁移的作用。所有这些结果表明 FSH 在调节内皮细胞方面具有功能作用。
