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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Regulation of human trophoblast migration and invasiveness.
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Regulation of human trophoblast migration and invasiveness.

机译：调节人类滋养细胞的迁移和侵袭性。

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The human placenta is an invasive structure in which highly proliferative, migratory, and invasive extravillous trophoblast (EVT) cells migrate and invade the uterus and its vasculature. Using in vitro propagated normal first-trimester EVT cells and immortalized EVT cells, which share all of the phenotypic and functional characteristics of the normal EVT cells, it has been shown that migration/invasion of human EVT cells is stringently regulated by many growth factors, their binding proteins, extracellular matrix (ECM) components, and some adhesion molecules in an autocrine/paracrine manner at the fetal-maternal interface in human pregnancy. Transforming growth factor beta (TGF-beta), decorin (a proteoglycan in the ECM), and melanoma cell adhesion molecule (Mel-CAM) inhibit, and insulin-like growth factor II (IGF-II), IGF-binding protein 1 (IGFBP-1), and endothelin 1 (ET-1) stimulate EVT cell migration/invasion. Inhibition of EVT cell migration by TGF-beta has been suggested to be due to upregulation of integrins, which make the cells more adhesive to the ECM. Its antiinvasive action is due to an upregulation of tissue inhibitor of matrix metalloprotease 1 (TIMP-1) and plasminogen activator inhibitor (PAI-1) and a downregulation of urokinase-type plasminogen activator (uPA). Molecular mechanisms of inhibition of migration/invasion of EVT cells by decorin and Mel-CAM remain to be identified. IGF-II action has been shown to be mediated by IGF type I receptors (IGF-RII) independently of IGF type I receptors (IGF-RI) and IGFBPs. This action of IGF-II appears to involve inhibitory G proteins and phosphorylation of mitogen-activated protein kinase (MAPK) (extracellular signal-regulated protein kinases 1 and 2 (ERK-1 and ERK-2)). IGFBP-1 stimulation of EVT cell migration appears to occur by binding its Arg-Gly-Asp (RGD) domain to alpha5beta1 integrin, leading to phosphorylation of focal adhesion kinase (FAK) and MAPK (ERK-1 and ERK-2). These studies may improve our understanding of diseases related to abnormal placentation, viz. hypoinvasiveness in preeclampsia and hyperinvasiveness in trophoblastic neoplasms.
机译：人胎盘是一种侵入性结构，高度增殖，迁移和侵入性绒毛外滋养层细胞（EVT）在其中迁移并侵入子宫及其脉管系统。使用具有正常EVT细胞所有表型和功能特征的体外繁殖的正常早孕EVT细胞和永生化EVT细胞，已证明人类EVT细胞的迁移/侵袭受到许多生长因子的严格调控，它们的结合蛋白，细胞外基质（ECM）成分和一些粘附分子以自分泌/旁分泌的方式在人类妊娠的胎儿-母亲界面处。转化生长因子beta（TGF-beta），decorin（ECM中的蛋白聚糖）和黑色素瘤细胞粘附分子（Mel-CAM）受到抑制，胰岛素样生长因子II（IGF-II），IGF结合蛋白1（ IGFBP-1）和内皮素1（ET-1）刺激EVT细胞迁移/侵袭。 TGF-β对EVT细胞迁移的抑制作用被认为是由于整联蛋白的上调，这使细胞对ECM的粘附性更高。它的抗侵袭作用是由于基质金属蛋白酶1（TIMP-1）和纤溶酶原激活物抑制剂（PAI-1）的组织抑制剂上调，以及尿激酶型纤溶酶原激活物（uPA）的下调。由decorin和Mel-CAM抑制EVT细胞迁移/侵袭的分子机制仍有待确定。 IGF-II的作用已被证明是由IGF I型受体（IGF-RII）介导的，而与IGF I型受体（IGF-RI）和IGFBP无关。 IGF-II的这种作用似乎涉及抑制性G蛋白和促分裂原活化蛋白激酶（MAPK）（细胞外信号调节蛋白激酶1和2（ERK-1和ERK-2））的磷酸化。 IGFBP-1刺激EVT细胞迁移似乎是通过将其Arg-Gly-Asp（RGD）域与alpha5beta1整联蛋白结合而发生的，从而导致粘着斑激酶（FAK）和MAPK（ERK-1和ERK-2）磷酸化。这些研究可以增进我们对与异常胎盘相关疾病的了解。子痫前期的侵袭性低和滋养细胞肿瘤的侵袭性高。

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