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子宫自然杀伤细胞:早期基蜕膜血管构建的监督者。

Uterine natural killer cells: supervisors of vasculature construction in early decidua basalis.

作者信息

Rätsep Matthew T, Felker Allison M, Kay Vanessa R, Tolusso Leandra, Hofmann Alexander P, Croy B Anne

机构信息

Department of Biomedical and Molecular SciencesQueen's University, Botterell Hall, Room 926, 18 Stuart Street, Kingston, Ontario, Canada K7L3N6

Department of Biomedical and Molecular SciencesQueen's University, Botterell Hall, Room 926, 18 Stuart Street, Kingston, Ontario, Canada K7L3N6.

出版信息

Reproduction. 2015 Feb;149(2):R91-102. doi: 10.1530/REP-14-0271. Epub 2014 Oct 23.

DOI:10.1530/REP-14-0271
PMID:25342175
Abstract

Mammalian pregnancy involves tremendous de novo maternal vascular construction to adequately support conceptus development. In early mouse decidua basalis (DB), maternal uterine natural killer (uNK) cells oversee this process directing various aspects during the formation of supportive vascular networks. The uNK cells recruited to early implantation site DB secrete numerous factors that act in the construction of early decidual vessels (neoangiogenesis) as well as in the alteration of the structural components of newly developing and existing vessels (pruning and remodeling). Although decidual and placental development sufficient to support live births occur in the absence of normally functioning uNK cells, development and structure of implantation site are optimized through the presence of normally activated uNK cells. Human NK cells are also recruited to early decidua. Gestational complications including recurrent spontaneous abortion, fetal growth restriction, preeclampsia, and preterm labor are linked with the absence of human NK cell activation via paternally inherited conceptus transplantation antigens. This review summarizes the roles that mouse uNK cells normally play in decidual neoangiogenesis and spiral artery remodeling in mouse pregnancy and briefly discusses changes in early developmental angiogenesis due to placental growth factor deficiency.

摘要

哺乳动物的怀孕涉及母体大量的新生血管构建,以充分支持胚胎发育。在小鼠早期的基底蜕膜(DB)中,母体子宫自然杀伤(uNK)细胞负责监督这一过程,在支持性血管网络形成过程中指导各个方面。招募到早期着床部位DB的uNK细胞分泌多种因子,这些因子在早期蜕膜血管构建(新生血管形成)以及新发育血管和现有血管结构成分的改变(修剪和重塑)中发挥作用。尽管在没有正常功能的uNK细胞的情况下也会发生足以支持活产的蜕膜和胎盘发育,但通过正常激活的uNK细胞的存在,着床部位的发育和结构得以优化。人类NK细胞也会被招募到早期蜕膜。包括复发性自然流产、胎儿生长受限、子痫前期和早产在内的妊娠并发症与通过父系遗传的胚胎移植抗原导致的人类NK细胞激活缺失有关。本综述总结了小鼠uNK细胞在小鼠妊娠蜕膜新生血管形成和螺旋动脉重塑中通常发挥的作用,并简要讨论了由于胎盘生长因子缺乏导致的早期发育血管生成的变化。

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