期刊
JOURNAL OF IMMUNOLOGY
卷 185, 期 7, 页码 4420-4429出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0903215
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资金
- European Network of Excellence on Embryo Implantation Control [512040]
- Associazione Italiana per la Ricerca sul Cancro
- Italian Federation for Cancer Research
- Italian Ministry of University and Research [FIRB RBIN045LT8, PRIN 2007]
- Regione Friuli-Venezia Giulia
- National Institutes of Health [AI 060866]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI060866] Funding Source: NIH RePORTER
Fetal trophoblast cells invading the decidua in the early phase of pregnancy establish complex interaction with the maternal extracellular matrix. We discovered that C1q was widely distributed in human decidual stroma in the absence of C4 and C3 and was actively synthesized by migrating extravillous trophoblasts. The cells expressed the messages for the three chains of C1q and secreted this complement component that interacted with the proteins of the decidual extracellular matrix. Solid phase-bound C1q promoted trophoblast adhesion and migration, and cell binding to C1q resulted in activation of ERK1/2 MAPKs. Ab inhibition experiments showed that the receptors for the globular head of C1q/p33 and alpha(4)beta(1) integrin were both involved in this process and were colocalized on the cell surface following binding of C1q to trophoblasts. We also found that C1q(-/-) mice manifested increased frequency of fetal resorption, reduced fetal weight, and smaller litter sizes compared with wild-type mice. C1q deficiency was associated with impaired labyrinth development and decidual vessel remodeling. Collectively, these data suggest that C1q plays an important role in promoting trophoblast invasion of decidua and that defective local production of C1q may be involved in pregnancy disorders, such as pre-eclampsia, characterized by poor trophoblast invasion. The Journal of Immunology, 2010, 185: 4420-4429.
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