A non-redundant role of complement protein C1q in normal and adverse pregnancy

C. Agostinis, A. Mangogna, A. Balduit, U. Kishore, R. Bulla
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Abstract

Complement component 1q (C1q) is the recognition molecule of the classical pathway of the complement system that can bind to an array of closely spaced antigen-bound immunoglobulin G (IgG) and IgM antibodies. In addition to its involvement in defence against a range of pathogens and clearance of apoptotic and necrotic cells, C1q has also been implicated in immune and non-immune homeostasis. C1q is locally produced by immune cells such as monocytes, macrophages, and dendritic cells. C1q is also synthesized by decidual endothelial cells, thus acting as a link between decidual cells and trophoblasts, as well as contributing to the remodelling of spiral arteries. Furthermore, C1q is produced by the extravillous trophoblasts (EVTs) invading the decidua. As a pro-angiogenic molecule, C1q is also important for normal placentation processes as it favors the active angiogenesis in the developing decidua. These observations have been validated by C1q gene knock-out mice which showed pre-eclampsia (PE)-like symptoms, characterized by hypertension, proteinuria, glomerular endotheliosis, and increased soluble fms-like tyrosine kinase-1 (sFlt-1)/placental growth factor (PlGF) ratio, and increased oxidative stress. The role of C1q in normal and adverse human pregnancy is being studied extensively due to its absence or low level as a likely precipitating factor for the development of PE.
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补体蛋白C1q在正常和不良妊娠中的非冗余作用
补体成分1q (C1q)是补体系统经典途径的识别分子,可以结合一系列紧密间隔的抗原结合免疫球蛋白G (IgG)和IgM抗体。除了参与防御一系列病原体和清除凋亡和坏死细胞外,C1q还与免疫和非免疫稳态有关。C1q由免疫细胞如单核细胞、巨噬细胞和树突状细胞局部产生。C1q也可由蜕膜内皮细胞合成,作为蜕膜细胞与滋养层细胞之间的纽带,参与螺旋动脉的重塑。此外,C1q是由侵入蜕膜的胞外滋养细胞(evt)产生的。作为一种促血管生成分子,C1q对正常胎盘过程也很重要,因为它有利于发育中的蜕膜中活跃的血管生成。这些观察结果被C1q基因敲除的小鼠证实,这些小鼠表现出先兆子痫(PE)样症状,其特征是高血压、蛋白尿、肾小球内皮增生、可溶性膜样酪氨酸激酶-1 (sFlt-1)/胎盘生长因子(PlGF)比例增加,氧化应激增加。C1q在正常和不良妊娠中的作用正在被广泛研究,因为它缺乏或低水平可能是PE发展的促成因素。
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