LAMA5 promotes human umbilical vein endothelial cells migration, proliferation, and angiogenesis and is decreased in preeclampsia.

Objective: Preeclampsia (PE) is currently thought to associated with oxidative stress and vascular endothelial dysfunction. LAMA5 is associated with the cell migration, proliferation, and vascular endothelial function. The aims of this study are to investigate the expression patterns of LAMA5 in normal and PE pregnancies, as well as evaluating the effects of LAMA5 on human umbilical vein endothelial cells (HUVECs) function.Methods: LAMA5 expression levels were examined by reverse-transcriptase polymerase chain reaction (RT-PCR) and further confirmed by western blot and immunofluorescence. Cell proliferation and apoptosis were measured by CCK-8 assay and flow cytometry respectively. Cell migration was assessed by transwell migration assay.Results: LAMA5 expression levels of vascular endothelial cells in PE placentas was significantly decreased than that in normal placentas. LAMA5 small-interfering RNA (siRNA) transfection and hypoxia/reoxygenation (H/R) treatments resulted in decreased proliferation, migration, and vascular formation ability of HUVECs but increased HUVECs apoptosis. Down-regulated LAMA5 could inhibit the protein expression of the PI3K downstream p-AKT and p-MTOR.Conclusions: Down-regulated LAMA5 is associated with PE placenta and restrained HUVECs proliferation, migration, and angiogenesis through PI3K-AKT-MTOR signaling pathways.