Journal
JOURNAL OF REPRODUCTIVE IMMUNOLOGY
Volume 119, Issue -, Pages 74-80Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.jri.2016.09.001
Keywords
Innate immunity; Complement system; C1 q; Trophoblast invasion; Pre-eclampsia
Categories
Funding
- Institute for Maternal and Child Health, IRCCS Burlo Garofolo, Trieste, Italy [RC41/08 RC 01/09 RC 34/11]
- European NoE EMBIC within FP6 [LSHN-CT-2004-512040]
- Fondazione Cassa di Risparmio di Trieste
- Fondazione Casali
Ask authors/readers for more resources
Complement component C1q is one of the recognition molecules of the complement system which can serve several functions unrelated to complement activation. This molecule is produced at foeto-maternal interface by macrophages as wells as by decidual endothelial cells and invading trophoblast. Foetal trophoblast cells migrating through the decidua in the early stages of pregnancy synthesize and express C1q on their surface, which is actively involved in promoting trophoblast endovascular and interstitial invasion of the decidua. These functions are mediated by two cell surface receptors, gC1qR and alpha 4 beta 1 integrin, which promote trophoblast adhesion and migration through the activation of ERK1/2 MAPKs. C1q(-/-) mice manifest increased frequency of foetal resorption, reduced foetal weight, and smaller litter size when compared to their wild-type counterparts, suggesting that defective local production of C1q maybe involved in pregnancy disorders, such as pre-eclampsia. C1q acts also as a strong angiogenic factor and promotes neovascularization. These studies suggest novel and unexpected roles of this complement component in physiological and pathological pregnancies. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available