Abstract
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.