GNA11 differentially mediates fibroblast growth factor 2‐ and vascular endothelial growth factor A‐induced cellular responses in human fetoplacental endothelial cells

摘要

Key points class="unordered" style="list-style-type:disc" id="tjp12963-list-0001">Fetoplacental vascular growth is critical to fetal growth. Fibroblast growth factor 2 (FGF2) and vascular endothelial growth factor A (VEGFA) are two major regulators of fetoplacental vascular growth. G protein α subunit 11 (GNA11) transmits signals from many external stimuli to the cellular interior and may mediate endothelial function.It is not known whether GNA11 mediates FGF2‐ and VEGFA‐induced endothelial cell responses under physiological chronic low O2.In the present study, we show that knockdown of GNA11 significantly decreases FGF2‐ and VEGFA‐induced fetoplacental endothelial cell migration but not proliferation and permeability.Such decreases in endothelial migration are associated with increased phosphorylation of phospholipase C‐β3.The results of the present study suggest differential roles of GNA11 with respect to mediating FGF2‐ and VEGFA‐induced fetoplacental endothelial function.