Abstract

Preeclampsia (PE) is a common disease among pregnant women and is characterized by high blood pressure, edemas, proteinuria, etc. However, the underlying mechanism of PE is still not clear. Our results may provide a new understanding of the pathogenesis of PE and a therapeutical target for the treatment of the disease. Levels of long intergenic ncRNA 00473 (LINC00473), miR-16-5p, MMP2, MMP9, Bcl-2, Bax, and C caspase-3 in placental tissues or human trophoblastic cells were assessed. HTR8/SVneo and JEG-3 cells were transfected with LINC00473, miR-16-5p mimic, LINC00473 siRNA, or miR-16-5p inhibitor alone, or co-transfected with LINC00473 and miR-16-5p mimic or LINC00473 siRNA and miR-16-5p inhibitor. Viability, apoptosis, migration and invasion of cells were assessed by Cell Counting Kit-8, flow cytometry, wound healing assay and Transwell assay, respectively. The target gene of LINC00473 was analyzed using Starbase and dual-luciferase reporter assay. LINC00473 level was down-regulated in placental tissues of PE patients. LINC00473 overexpression increased cell viability, migration, invasion, and MMP2, MMP9 and Bcl-2 levels, yet decreased the apoptosis rates and Bax and C caspase-3 levels in cells; however, LINC00473 silencing had the opposite effect. LINC00473 targeted miR-16-5p and miR-16-5p level was negatively related to LINC00473 level. MiR-16-5p mimic reversed the promoting effect of LINC00473 overexpression on the invasion of HTR8/SVneo and JEG-3 cells, while miR-16-5p inhibitor reversed the inhibitory effect of LINC00473 silencing on the invasion of these cells. In conclusion, LINC00473 improved the invasion of human trophoblastic cells via miR-16-5p.