MALAT1/CREG1通过自噬介导的羊膜成纤维细胞分化调控胎膜早破的机制

IF 5.9 3区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Non-coding RNA Research Pub Date : 2025-04-10 DOI:10.1016/j.ncrna.2025.04.004

Xiaomei Huang , Ting Huang , Aixing Chen , Yong Shao

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引用次数: 0

摘要

背景胎膜早破是早产的主要原因之一。羊膜在负重过程中起着重要的作用，而羊膜成纤维细胞也起着重要的作用。本研究旨在探讨成纤维细胞介入羊膜早破修复相关的科学问题，为临床治疗羊膜早破提供依据。方法课课组通过单细胞测序、天狼星染色、荧光染色、拉曼光谱等方法对胎儿膜组织进行实验，探索胎儿膜结构的变化，并通过WB、PCR、RNA Pulldown、RIP、分子对接等实验验证临床组织和原代成纤维细胞中的关键靶点和通路。结果胎膜早破组胎膜结构明显受损，羊膜成纤维细胞被激活，自噬被激活，自噬激活促进成纤维细胞活化。转移相关肺腺癌转录本1 （MALAT1）在羊膜成纤维细胞中的表达显著升高。RNA PULL DOWN和分子对接结果提示MALAT1结合人E1A启动子抑制因子1 （CREG1）并促进自噬。结论MALAT1通过与CREG1相互作用，增加CREG1的表达，调节自噬相关分子的表达，介导羊膜成纤维细胞向肌成纤维细胞分化，参与羊膜修复，促进早膜胎膜组织修复。

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

Background

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.

Methods

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.

Results

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.

Conclusions

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.

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来源期刊

Non-coding RNA Research Medicine-Biochemistry (medical)

CiteScore

7.70

自引率

6.00%

发文量

审稿时长

49 days

期刊介绍： Non-coding RNA Research aims to publish high quality research and review articles on the mechanistic role of non-coding RNAs in all human diseases. This interdisciplinary journal will welcome research dealing with all aspects of non-coding RNAs-their biogenesis, regulation and role in disease progression. The focus of this journal will be to publish translational studies as well as well-designed basic studies with translational and clinical implications. The non-coding RNAs of particular interest will be microRNAs (miRNAs), small interfering RNAs (siRNAs), small nucleolar RNAs (snoRNAs), U-RNAs/small nuclear RNAs (snRNAs), exosomal/extracellular RNAs (exRNAs), Piwi-interacting RNAs (piRNAs) and long non-coding RNAs. Topics of interest will include, but not limited to: -Regulation of non-coding RNAs -Targets and regulatory functions of non-coding RNAs -Epigenetics and non-coding RNAs -Biological functions of non-coding RNAs -Non-coding RNAs as biomarkers -Non-coding RNA-based therapeutics -Prognostic value of non-coding RNAs -Pharmacological studies involving non-coding RNAs -Population based and epidemiological studies -Gene expression / proteomics / computational / pathway analysis-based studies on non-coding RNAs with functional validation -Novel strategies to manipulate non-coding RNAs expression and function -Clinical studies on evaluation of non-coding RNAs The journal will strive to disseminate cutting edge research, showcasing the ever-evolving importance of non-coding RNAs in modern day research and medicine.