C5a receptor signaling prevents folate deficiency-induced neural tube defects in mice.
C5a receptor signaling prevents folate deficiency-induced neural tube defects in mice.
复制标题
DOI：
10.4049/jimmunol.1203072
复制
发表时间：
2013-04-01
期刊：
影响因子：
--
通讯作者：
Taylor SM
中科院分区：
文献类型：
--
作者：
Denny KJ;Coulthard LG;Jeanes A;Lisgo S;Simmons DG;Callaway LK;Wlodarczyk B;Finnell RH;Woodruff TM;Taylor SM
补体系统参与一系列不同的发育过程，包括细胞存活、生长、分化和再生。然而，关于补体在胚胎发生中的作用知之甚少。在这里，我们证明了一个新的作用，典型的补体5a受体（C5aR）在哺乳动物神经管的发展条件下，母亲的饮食叶酸缺乏。具体而言，我们发现C5aR和C5在野生型小鼠神经形成的整个时期表达，并将表达定位于发育中的神经管的头部区域。C5aR在人早期胚胎的神经上皮中也有表达。切除C5ar1基因或给予特定的C5aR肽拮抗剂叶酸缺乏的怀孕小鼠导致严重的前神经管缺陷相关的先天性畸形的高患病率。这些发现为补体系统在哺乳动物胚胎发育过程中的作用提供了一个新的和令人信服的见解。
The complement system is involved in a range of diverse developmental processes including cell survival, growth, differentiation, and regeneration. However, little is known about the role of complement in embryogenesis. Herein we demonstrate a novel role for the canonical complement 5a receptor (C5aR) in the development of the mammalian neural tube under conditions of maternal dietary folic acid deficiency. Specifically, we found C5aR and C5 to be expressed throughout the period of neurulation in wildtype mice and localized the expression to the cephalic regions of the developing neural tube. C5aR was also found to be expressed in the neuroepithelium of early human embryos. Ablation of the C5ar1 gene or the administration of a specific C5aR peptide antagonist to folic acid-deficient pregnant mice resulted in a high prevalence of severe anterior neural tube defect-associated congenital malformations. These findings provide a new and compelling insight into the role of the complement system during mammalian embryonic development.
登录
查看更多内容
影响因子：
4.4
作者：
Kildsgaard, J;Hollmann, TJ;Wetsel, RA
通讯作者：
Wetsel, RA
影响因子：
4.8
作者：
Pavlovski, Dale;Thundyil, John;Woodruff, Trent M.
通讯作者：
Woodruff, Trent M.
影响因子：
3.5
作者：
Juriloff, DM;Harris, MJ
通讯作者：
Harris, MJ
影响因子：
5.2
作者：
SMITHELLS, RW;SHEPPARD, S;SCHORAH, CJ
通讯作者：
SCHORAH, CJ
影响因子：
56.9
作者：
Fleming, A;Copp, AJ
通讯作者：
Copp, AJ