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 amniot...
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KeAi Communications Co., Ltd.
2025-08-01
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| Series: | Non-coding RNA Research |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2468054025000435 |
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| author | Xiaomei Huang Ting Huang Aixing Chen Yong Shao |
| author_facet | Xiaomei Huang Ting Huang Aixing Chen Yong Shao |
| author_sort | Xiaomei Huang |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-d29b4c5064d8407094715fa852eeca87 |
| institution | DOAJ |
| issn | 2468-0540 |
| language | English |
| publishDate | 2025-08-01 |
| publisher | KeAi Communications Co., Ltd. |
| record_format | Article |
| series | Non-coding RNA Research |
| spelling | doaj-art-d29b4c5064d8407094715fa852eeca872025-08-20T03:15:42ZengKeAi Communications Co., Ltd.Non-coding RNA Research2468-05402025-08-0113294210.1016/j.ncrna.2025.04.004The mechanism by which MALAT1/CREG1 regulates premature rupture of fetal membrane through autophagy mediated differentiation of amniotic fibroblastsXiaomei Huang0Ting Huang1Aixing Chen2Yong Shao3Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, ChinaDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China; Department of Obstetrics and Gynecology, Chongqing Health Center for Women and Children, Women and Children's Hospital of Chongqing Medical University, Chongqing, 400016, ChinaDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, ChinaDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China; Corresponding author.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.http://www.sciencedirect.com/science/article/pii/S2468054025000435Premature rupture of fetal membraneMetastasis-associated lung adenocarcinoma transcript 1AutophagyFibroblasts |
| spellingShingle | Xiaomei Huang Ting Huang Aixing Chen Yong Shao The mechanism by which MALAT1/CREG1 regulates premature rupture of fetal membrane through autophagy mediated differentiation of amniotic fibroblasts Non-coding RNA Research Premature rupture of fetal membrane Metastasis-associated lung adenocarcinoma transcript 1 Autophagy Fibroblasts |
| title | The mechanism by which MALAT1/CREG1 regulates premature rupture of fetal membrane through autophagy mediated differentiation of amniotic fibroblasts |
| title_full | The mechanism by which MALAT1/CREG1 regulates premature rupture of fetal membrane through autophagy mediated differentiation of amniotic fibroblasts |
| title_fullStr | The mechanism by which MALAT1/CREG1 regulates premature rupture of fetal membrane through autophagy mediated differentiation of amniotic fibroblasts |
| title_full_unstemmed | The mechanism by which MALAT1/CREG1 regulates premature rupture of fetal membrane through autophagy mediated differentiation of amniotic fibroblasts |
| title_short | The mechanism by which MALAT1/CREG1 regulates premature rupture of fetal membrane through autophagy mediated differentiation of amniotic fibroblasts |
| title_sort | mechanism by which malat1 creg1 regulates premature rupture of fetal membrane through autophagy mediated differentiation of amniotic fibroblasts |
| topic | Premature rupture of fetal membrane Metastasis-associated lung adenocarcinoma transcript 1 Autophagy Fibroblasts |
| url | http://www.sciencedirect.com/science/article/pii/S2468054025000435 |
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