Abstract:
BACKGROUND:Spontaneous abortion is a common disease in human pregnancy. Increasing evidence suggests that proper function of trophoblasts and immune balance of the maternal-fetal interface are crucial for successful pregnancy. Macrophages are involved in the maternal-fetal immune microenvironment. However, mechanisms associated with how macrophages impair trophoblasts' function in spontaneous abortion remain to be explored. METHODS:Firstly, the characteristics of the isolated macrophage-derived exosomes were verified by TEM and Western blot. Then, we established the co-culture of macrophage-derived exosomes with trophoblasts, and explored the role of the exosomes in trophoblasts. Moreover, expression of miR-153-3p in the macrophage-derived exosomes was detected. A miR-153-3p mimic was transfected into trophoblasts to investigate its function in the biological functions of trophoblast cells. MRNA and protein expressions were detected by qRT-PCR and Western blot. CCK8 assay was performed to measure cell proliferation and Transwell assay was utilized to examine migration of trophoblasts. RESULTS:Compared with those in normal pregnant women, decidual macrophage-derived exosomes from unexplained recurrent spontaneous abortion (URSA) patients suppressed the proliferation and migration of trophoblast cells through the IDO/STAT3 pathway. MiR-153-3p was highly expressed in exosomes released from decidual macrophages of URSA patients. Transfecting miR-153-3p mimics into trophoblast cells directly inhibited IDO genes, which suppressed STAT3 pathway activation, regulating the biological behavior of trophoblast cells. CONCLUSIONS:This study outlines the role of decidual macrophage-derived exosomal miR-153-3p in successful pregnancy maintenance, paving a new approach for the development of novel treatments for URSA.
journal_name
Int Immunopharmacoljournal_title
International immunopharmacologyauthors
Ying X,Jin X,Zhu Y,Liang M,Chang X,Zheng Ldoi
10.1016/j.intimp.2020.106981subject
Has Abstractpub_date
2020-11-01 00:00:00pages
106981eissn
1567-5769issn
1878-1705pii
S1567-5769(20)31308-4journal_volume
88pub_type
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