Upregulated endoplasmic reticulum oxidoreductin 1-like protein alpha at the mother-fetus interface of preeclampsia promotes trophoblast cell migration and invasion.

Endoplasmic reticulum oxidoreductin 1-like protein alpha (ERO1A) is a disulfide oxidoreductase involved in the formation of protein disulfide bonds. However, the relationship between ERO1A and preeclampsia onset remains unclear. The aim of this study was therefore to clarify the role of ERO1A in regulating trophoblast cell migration and invasion. Placental tissues were collected from participants with normal pregnancies (n = 17) and pre-eclampsia (n = 15). Immunohistochemistry was performed to detect the expression and localization of ERO1A. Next, stable cell lines with ERO1A overexpression and knockout were constructed in human trophoblast cells (HTR-8/SVneo). HTR-8/SVneo migration and invasion were then detected using Transwell assays. The ability of trophoblasts to invade the endothelial tube was analyzed using DiO- and DiI-stained cells. Finally, ERO1A and collagen type III alpha 1 (COL3A1) expression was detected using Western blotting. Our results showed that ERO1A expression was significantly upregulated in the villous tissues of women with early-onset preeclampsia. Overexpression of ERO1A promoted HTR-8/SVneo cell invasion, the ability to penetrate the endothelial tube, and enhanced the expression of COL3A1. Our findings suggest that high ERO1A expression in early-onset preeclampsia plays a protective role in alleviating disease progression.