ArticleReproductive sciences (Thousand Oaks, Calif.)2023
Combined Application of Exosomes and FPR2 Agonist LXA4 in Controlling Fetal Membrane Inflammation and Promoting Fetal Membrane Tissue Repair.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Noninvasive PPROM risk stratification with explainable AI using routine antenatal CRP and albumin.NPJ digital medicine · 2026Article
- Research progress and prospects of exosomes from diverse cellular sources in the treatment of knee osteoarthritis: a narrative review.Frontiers in surgery · 2026Review
- Lipoxins as Modulators of Diseases.Cells · 2025Review
- The mechanism by which MALAT1/CREG1 regulates premature rupture of fetal membrane through autophagy mediated differentiation of amniotic fibroblasts.Non-coding RNA research · 2025Article
- Application of adult stem cells in obstetrics and gynecology: A scoping review.European journal of obstetrics & gynecology and reproductive biology: X · 2025Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Preterm premature rupture of membranes (pPROM) is a common pregnancy disease closely related to inflammation. The formyl peptide receptor 2 (FPR2), a member of the G protein-coupled receptor family involved in defense responses, inflammation, and disturbances in glucose and lipid metabolism, is associated with pregnancy diseases. Lipoxin A4 (LXA4) can activate FPR2 and inhibit the inflammatory signals. Exosomes derived from mesenchymal stem cells are good materials for anti-inflammatory and tissue repair. This study aims to investigate the anti-inflammatory and tissue repair effects of the combined application of exosomes derived from human umbilical cord mesenchymal stem cells and FPR2 agonist LXA4. In this study, LPS was used to establish the inflammation model of pregnant mice and HTR8 cells, and LXA4 and exosome treatment were carried out to observe the fetal membranes' tissue repair. The scanning and transmission electron microscopy of fetal membrane tissue indicated that the structure of pPROM tissue was disordered, and the cell gap was significantly increased. The results of the inflammatory mice model suggested that LPS can cause damage to the fetal membrane structure. LXA4 combined with exosome treatment can inhibit the production of MMP2 and MMP9, and promote neovascularization by inhibiting the p38 MAPK/Nuclear factor kB p65 (NFkB) pathway in the inflammation model of HTR8 cells and pregnant mice, thus helping to control inflammation and tissue repair.
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