Hormonal regulation of uterine natural killer cells in mouse preimplantation uterus

Hormonal regulation of uterine natural killer cells in mouse preimplantation uterus
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小鼠着床前子宫中子宫自然杀伤细胞的激素调节

DOI:
10.1007/s10735-010-9256-8
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发表时间:
2010-02-01
影响因子:
3.2
通讯作者:
Tan, Yi
Tan, Yi
中科院分区:
生物学4区
文献类型:
--
作者:
Kuang, Haibin;Peng, Hongying;Tan, Yi

文献摘要

被引文献

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子宫自然杀伤(uNK)细胞是小鼠和人类妊娠期间子宫中募集的最丰富的淋巴细胞群。以往对小鼠妊娠期uNK细胞的研究主要集中在着床后的积累,认为其在滋养层细胞侵袭和血管生成中起重要作用,从而促进胎盘形成。然而,通过使用最近开发的双花扁豆凝集素(DBA)凝集素的方法,在小鼠着床前进行更仔细的检查发现,uNK细胞也存在动态调节,这表明类固醇激素的主要调节。在这里,我们提供了一个详细的检查uNK细胞分布在小鼠早期妊娠DBA凝集素反应,重点是着床前时期及其激素调节配置文件。我们的研究结果表明,uNK前体细胞或其细胞膜特异性成分可以招募在子宫内的雌激素或/和孕激素,其作用可以完全消除其核受体(雌激素和孕激素受体)的特异性拮抗剂。这些结果提示,着床前子宫通过激素的协同调节,可以募集uNK前体细胞或其特异性细胞成分,这可能有助于子宫的容受性和着床后uNK的进一步构建/功能。
Uterine Natural Killer (uNK) cells are the most abundant lymphocyte population recruited in the uteri during murine and human pregnancy. Previous investigation on uNK cells during mouse pregnancy focused more on its accumulation in postimplantation periods, which were believed to play important roles in regulating trophoblast invasion and angiogenesis towards successful placentation. However, by using recently developed methods of Dolichos biflorus agglutinin (DBA) lectin, a closer examination during mouse preimplantation revealed that there were also dynamic regulations of uNK cell, suggesting a major regulation by steroid hormones. Here we provide a detailed examination of uNK cells distribution during mouse early pregnancy by DBA lectin reactivity, with emphasis on preimplantation period and its hormonal regulation profiles. Our results showed that uNK precursor cells or its cell membrane specific components could be recruited in the uterus by estrogen or/and progesterone, and the effects could be completely abolished by specific antagonists of their nuclear receptors (estrogen and progesterone receptor). These results suggested that the preimplantation uterus, through concerted hormone regulation, could recruit uNK precursor cell or its specific cellular component, which might be conducive for uterine receptivity and further uNK construction/function during postimplantation.