Combined Application of Exosomes and FPR2 Agonist LXA4 in Controlling Fetal Membrane Inflammation and Promoting Fetal Membrane Tissue Repair
作者全名:"Huang, Xiaomei; Liao, Junqun; Feng, Fan; Chen, Siyu; Liao, E.; Li, Dong; Dai, Xiaoyu; Dong, Jing; Shao, Yong"
作者地址:"[Huang, Xiaomei; Feng, Fan; Chen, Siyu; Liao, E.; Shao, Yong] Chongqing Med Univ, Affiliated Hosp 1, Dept Obstet & Gynecol, Chongqing 400042, Peoples R China; [Liao, Junqun] Chongqing Med Univ, Affiliated Hosp 1, Med Lab Sci, Chongqing 400042, Peoples R China; [Liao, E.] Maternal & Child Hlth Hosp Hubei Prov, Dept Obstet, Wuhan 430070, Hubei, Peoples R China; [Li, Dong] Shandong Univ, Cryomedicine Lab, Qilu Hosp, Jinan 250012, Shandong, Peoples R China; [Dai, Xiaoyu; Dong, Jing] Chongqing Perfect Cell Biotechnol Co LTD, Chongqing 400042, Peoples R China"
通信作者:"Shao, Y (通讯作者),Chongqing Med Univ, Affiliated Hosp 1, Dept Obstet & Gynecol, Chongqing 400042, Peoples R China."
来源:REPRODUCTIVE SCIENCES
ESI学科分类:CLINICAL MEDICINE
WOS号:WOS:000899932700001
JCR分区:Q2
影响因子:2.6
年份:2023
卷号:
期号:
开始页:
结束页:
文献类型:Article; Early Access
关键词:Preterm premature rupture of membranes; Formyl peptide receptor 2; Lipoxin A4; Exosomes
摘要:"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."
基金机构:National Natural Science Foundation of China; Chongqing Health Planning Commission project [81471473]; [2019ZDXM055]
基金资助正文:"This work is funded by National Natural Science Foundation of China (No: 81471473) and Chongqing Health Planning Commission project (No. 2019ZDXM055). This funding supported the design of the study and collection, analysis, and interpretation of data and writing of the manuscript."