Preeclampsia (PE) is associated with defective placental angiogenesis and poor placentation. Laminins are the main noncollagenous glycoproteins in basement membranes, and laminin α4 (LAMA4) promotes the migration, proliferation, and survival of various cells. The primary purpose of this study is to investigate the role of LAMA4 in human umbilical vein endothelial cells (HUVECs) function during the development of PE. We found expression levels of LAMA4 in human PE placentas were significantly lower compared to the control placentas. The LAMA4 small-interfering RNA transfection and hypoxia-reoxygenation (H/R) intervention reduced the migratory and tube formation abilities of HUVECs. The mitogen-activated protein kinase (MAPK) signaling pathways interacted with LAMA4 expression and H/Rexposure led to MAPK pathways activation in HUVECs. We demonstrated that LAMA4 is very crucial in promoting the functions of endothelial cells. Oxidative stress plays a vital role in controlling expression of LAMA4 through MAPK signaling pathways, which suggests a possible pathological mechanism of PE.
Keywords: laminin α4; oxidative stress; p38 mitogen-activated protein kinase; preeclampsia.
© The Author(s) 2015.