@article {10577,
	title = {Alternative functions of the complement protein C1q at embryo implantation site.},
	journal = {J Reprod Immunol},
	volume = {119},
	year = {2017},
	month = {2017 02},
	pages = {74-80},
	abstract = {<p>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 α4β1 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 may be 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.</p>},
	keywords = {Animals, Complement C1q, Decidua, Embryo Implantation, Extracellular Signal-Regulated MAP Kinases, Female, Humans, Integrin alpha4beta1, Mice, Mice, Knockout, Neovascularization, Physiologic, Pre-Eclampsia, Pregnancy, Trophoblasts, Vascular Remodeling},
	issn = {1872-7603},
	doi = {10.1016/j.jri.2016.09.001},
	author = {Agostinis, Chiara and Tedesco, Francesco and Bulla, Roberta}
}
@article {1615,
	title = {An alternative role of C1q in cell migration and tissue remodeling: contribution to trophoblast invasion and placental development.},
	journal = {J Immunol},
	volume = {185},
	year = {2010},
	month = {2010 Oct 1},
	pages = {4420-9},
	abstract = {<p>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 α(4)β(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.</p>},
	keywords = {Animals, Cell Adhesion, Chemotaxis, Leukocyte, Complement C1q, Female, Humans, Immunoblotting, Immunohistochemistry, Immunoprecipitation, Mice, Mice, Inbred C57BL, Microscopy, Confocal, Placentation, Pre-Eclampsia, Pregnancy, Reverse Transcriptase Polymerase Chain Reaction, Trophoblasts},
	issn = {1550-6606},
	doi = {10.4049/jimmunol.0903215},
	author = {Agostinis, Chiara and Bulla, Roberta and Tripodo, Claudio and Gismondi, Angela and Stabile, Helena and Bossi, Fleur and Guarnotta, Carla and Garlanda, Cecilia and De Seta, Francesco and Spessotto, Paola and Santoni, Angela and Ghebrehiwet, Berhane and Girardi, Guillermina and Tedesco, Francesco}
}
