Long noncoding RNA maternally expressed gene 3 improves trophoblast dysfunction and inflammation in preeclampsia through the Wnt/-Catenin/nod-like receptor pyrin domain-containing 3 axis.

Inadequate trophoblastic infiltration and resulting placental hypoxia and inflammation comprise the core pathological basis of preeclampsia (PE). Maternally expressed gene 3 () is known to be involved in the pathogenesis of preeclampsia by inhibiting the migration and invasion of trophoblasts and promoting their apoptosis. Nevertheless, the specific underlying downstream molecular mechanism of is less well characterized. In this study, we detected lower expression levels of and -Catenin and higher expression of nod-like receptor pyrin domain-containing 3 (NLRP3) in placental tissues of pregnant women with severe preeclampsia (sPE) than in normal pregnancies. Elevated serum levels of IL-1β and TNF-α were also observed in the sPE group. Then, we established a hypoxia/reoxygenation (H/R) model to mimic preeclampsia. Similar results with sPE group were found in the H/R group compared with the control group. In addition, suppressive trophoblast proliferation, migration and invasion and increases in the apoptotic rate and inflammation were also detected in the H/R group. Notably, overexpressing markedly improved trophoblast dysfunction and inflammation caused by H/R. However, the effects of on trophoblasts, whether upregulated or downregulated, can be reversed by DKK-1 (Wnt/-Catenin inhibitor) and MCC950 (NLRP3 inhibitor). The current study revealed that regulates trophoblast function and inflammation through the Wnt/-Catenin/NLRP3 axis and provided new insights into the pathogenesis of preeclampsia.