# The mechanism by which MALAT1/CREG1 regulates premature rupture of fetal membrane through autophagy mediated differentiation of amniotic fibroblasts

## TL;DR

This study explores how MALAT1 and CREG1 regulate autophagy in amniotic fibroblasts to repair fetal membranes in cases of premature rupture.

## Contribution

The study reveals a novel mechanism involving MALAT1/CREG1 interaction in autophagy-mediated amniotic membrane repair.

## Key findings

- PROM fetal membranes show structural damage and activated autophagy in amniotic fibroblasts.
- MALAT1 binds to CREG1, promoting autophagy and fibroblast differentiation into myofibroblasts.
- The MALAT1/CREG1 pathway contributes to fetal membrane repair and may aid in treating PROM.

## Abstract

Premature rupture of fetal membrane (PROM) is one of the main causes of premature delivery. The amniotic membrane plays a major role in bearing weight, and amniotic fibroblasts play an important role. The purpose of this study was to explore the scientific problems associated with amniotic membrane repair by intervening with fibroblasts to provide evidence for the clinical treatment of PROM.

This research group conducted experiments on fetal membrane tissue via single-cell sequencing, Sirius staining, fluorescence staining and Raman spectroscopy to explore changes in fetal membrane structure and verified key targets and pathways in clinical tissues and primary fibroblasts through WB, PCR, RNA Pulldown, RIP and molecular docking experiments.

The fetal membrane structure in the PROM group was obviously damaged, and the amniotic fibroblasts were activated and autophagy was activated, and the activated autophagy promoted the activation of fibroblasts. The expression of Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) was significantly increased in amniotic fibroblasts. RNA PULL DOWN and molecular docking results suggested that MALAT1 binds to human E1A promoter repressor 1 (CREG1) and promotes autophagy.

By interacting with CREG1, MALAT1 can increase the expression of CREG1, regulate the expression of autophagy-related molecules, mediate the differentiation of amniotic fibroblasts into myofibroblasts, participate in amniotic repair, and promote the repair of PROM fetal membrane tissue.