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首页> 美国卫生研究院文献>Experimental and Therapeutic Medicine >Upregulated unique long 16 binding protein 1 detected in preeclamptic placenta affects human extravillous trophoblast cell line (HTR-8/SVneo) invasion by modulating the function of uterine natural killer cells
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Upregulated unique long 16 binding protein 1 detected in preeclamptic placenta affects human extravillous trophoblast cell line (HTR-8/SVneo) invasion by modulating the function of uterine natural killer cells

机译：在子痫前期胎盘中检测到的独特的长16结合长蛋白1上调通过调节子宫自然杀伤细胞的功能影响人类绒毛外滋养层细胞系（HTR-8 / SVneo）的侵袭

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摘要

Well-controlled trophoblast invasion at the maternal-fetal interface is crucial for normal placentation and successful pregnancy, otherwise pathological conditions of pregnancy occur, such as preeclampsia. In previous studies, it has been demonstrated that unique long 16 binding protein (ULBP)1, a ligand for the natural-killer group (NKG)2D receptor on uterine natural killer (uNK) cells, is upregulated in the placenta in patients with preeclampsia. As they are present on the majority of the decidua, uNK have an important role in pregnancy. The aim of the present study was to determine the role of ULBP1 in trophoblast cell invasion, which is closely associated with the occurrence of preeclampsia. In the present study, ULBP1 expression levels in placentas collected after cesarean section from women with preeclampsia and normal pregnant women were determined by immunohistochemistry, reverse transcription-quantitative polymerase chain reaction and western blotting. The effects of ULBP1 on extravillous trophoblast cell line (HTR-8/SVneo) invasion mediated via uNK cells and the underlying mechanisms were investigated. mRNA and protein expression levels of ULBP1 were significantly upregulated (P<0.05) in preeclamptic placentas compared with normal controls. ULBP1 inhibited HTR-8/SVneo cells via the regulation of biological functions of uNK cells, including the downregulation of NKG2D expression on uNK cells and the stimulation of production of cytokines and chemokines that affect extravillous cytotrophoblast invasion by uNK cells. ULBP1 may have an important role in the pathophysiology of preeclampsia through the modification of biological functions of uNK cells, which may affect trophoblast invasion.
机译：母胎界面的滋养细胞浸润受到良好控制对于正常胎盘和成功妊娠至关重要，否则会发生妊娠的病理状况，例如先兆子痫。在先前的研究中，已经证明子痫前期患者的胎盘中独特的长16结合蛋白（ULBP）1，子宫自然杀伤（uNK）细胞上自然杀伤基团（NKG）2D受体的配体被上调。 。由于它们存在于大多数蜕膜中，因此uNK在怀孕中起着重要作用。本研究的目的是确定ULBP1在滋养细胞侵袭中的作用，其与先兆子痫的发生密切相关。在本研究中，通过免疫组织化学，逆转录-定量聚合酶链反应和免疫印迹测定了子痫前期妇女和正常孕妇剖宫产后胎盘中ULBP1的表达水平。研究了ULBP1对通过uNK细胞介导的绒毛外滋养层细胞系（HTR-8 / SVneo）侵袭的影响及其潜在机制。与正常对照组相比，先兆子痫胎盘中ULBP1的mRNA和蛋白表达水平显着上调（P <0.05）。 ULBP1通过调节uNK细胞的生物学功能来抑制HTR-8 / SVneo细胞，包括下调uNK细胞上NKG2D的表达以及刺激影响uNK细胞侵袭性绒毛外滋养细胞的细胞因子和趋化因子的产生。 ULBP1通过改变uNK细胞的生物学功能可能在子痫前期的病理生理中起重要作用，这可能会影响滋养细胞的侵袭。

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