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Updated: Oct 20, 2025

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
Published on: January 26, 2024
miR-519d downregulates LEP expression to inhibit preeclampsia development
Hairui Cai1, Dongmei Li1, Jun Wu1
1Obstetrics and Gynecology Department, Ningbo Women & Children's Hospital, No. 339, Liuting Road, Ningbo 315000, Zhejiang Province, People's Republic of China.
Abstract:
The purpose of the current study was to characterize role of microRNA (miR)-519d in trophoblast cells and preeclampsia (PE) development and its potential underlying mechanism. Regulation of leptin (LEP) by miR-519d was verified using a dual-luciferase reporter gene assay. Loss- and gain-of-function assays were conducted to detect the roles of miR-519d and LEP in proliferation, migratory ability, and invasive capacity of HTR-8/SVneo cells by means of CCK-8 assay, scratch test, and Transwell invasion assay, respectively. The cell apoptosis rate and cycle distribution were analyzed by flow cytometry. LEP expression was elevated, whereas miR-519d level was suppressed in the PE placenta samples compared with those from normal pregnancy. Depletion of LEP promoted proliferation, migratory ability, and invasive capacity and repressed apoptosis. miR-519d could bind 3' untranslated regions (3'UTRs) of LEP, the extent of which correlated negatively with LEP expression. miR-519d suppressed the expression of LEP in HTR-8/SVneo cells. Moreover, overexpression of miR-519d promoted survival and migratory ability of HTR-8/SVneo cells. Taken together, we find that miR-519d targeted LEP and downregulated its expression, which could likely inhibit the development of PE.
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