The regulatory role of the nuclear scaffold protein Emerin on the migration of amniotic epithelial cells and oxidative stress in a pressure environment

Abstract

Introduction

Preterm premature rupture of membranes (PPROM) significantly increases perinatal fetal mortality and neonatal morbidity. During PPROM progression, excessive amniotic fluid pressure accompanies oxidative stress (OS). The migration of amniotic epithelial cells (AECs) is crucial for PPROM repair. Cell migration and mechanotransduction are regulated by the nuclear skeleton protein Emerin. However, the effects of Emerin on fetal membrane healing, OS and nuclear signal transduction in a mechanical environment remain unknown.

Method

The AECs were subjected to hydrostatic pressures of 4 kPa (moderate) and 9 kPa (excessive), with 0 kPa serving as the control group. A series of experiments, including CCK-8 assay, ROS detection, RT-qPCR, and siRNA interference, were performed to investigate the potential role of Emerin in fetal membrane repair under pressure stimulation.

Results

Moderate pressure stimulation promoted the proliferation and migration of AECs, while excessive mechanical stimulation had an inhibitory effect. Pressure stimulation increased the intracellular ROS levels, and this effect was pressure-dependent. Pressure could regulate the expression of Emerin, thereby influencing nuclear deformation. When Emerin was knocked down, it caused nuclear retraction and enhanced nuclear deformation ability, promoting the migration and proliferation of AECs. Furthermore, knockdown of Emerin suppressed ROS production and rescued the cellular OS levels, which may occur through the activation of the Nrf2 signaling pathway.

Discussion

This study demonstrates the critical role of Emerin in regulating AECs migration and OS under pressure stimulation, suggesting its potential as a therapeutic target for PPROM repair.