# LncRNA UNC5C-AS1 inhibits angiogenesis and induces endothelial apoptosis via the miR-148a-3p/EMP1 axis in preeclampsia

## TL;DR

This study shows that the lncRNA UNC5C-AS1 helps reduce preeclampsia symptoms by regulating a key molecular pathway involving miR-148a-3p and EMP1.

## Contribution

The study identifies a novel regulatory mechanism involving UNC5C-AS1, miR-148a-3p, and EMP1 in preeclampsia.

## Key findings

- UNC5C-AS1 is downregulated in preeclampsia placentas and promotes endothelial cell functions.
- UNC5C-AS1 regulates HUVEC behavior through the miR-148a-3p/EMP1 axis.
- Overexpression of UNC5C-AS1 reduces tissue damage in a preeclampsia mouse model.

## Abstract

Preeclampsia (PE) is a severe pregnancy complication with unclear molecular mechanisms. Our research investigated the effect of UNC5C-AS1 on human umbilical vein endothelial cell (HUVEC) function in PE. UNC5C-AS1 was downregulated in PE placentas. Upregulating UNC5C-AS1 promoted HUVEC migration, invasion, tube formation, and the expression of vascular permeability factors, while UNC5C-AS1 silencing exhibited an opposite effect. UNC5C-AS1 directly targeted the miR148a3p/EMP1 axis. MiR-148a-3p was up-regulated and EMP1 was downregulated in PE. The regulatory effects of UNC5C-AS1 overexpression on HUVEC functions were reversed by miR-148a-3p mimics, and this reversal was subsequently rescued by EMP1 upregulation. UNC5C-AS1 overexpression ameliorated tissue damage in the PE mouse model. UNC5C-AS1 alleviated the PE-associated injury and modulated HUVEC function by targeting miR-148a-3p/EMP1 axis.