Preeclampsia is associated with failure of human cytotrophoblasts to mimic a vascular adhesion phenotype - One cause of defective endovascular invasion in this syndrome?
Preeclampsia is associated with failure of human cytotrophoblasts to mimic a vascular adhesion phenotype - One cause of defective endovascular invasion in this syndrome?
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DOI：
10.1172/jci119388
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发表时间：
1997-05-01
影响因子：
15.9
通讯作者：
Fisher, SJ
中科院分区：
文献类型：
--
作者：
Zhou, Y;Damsky, CH;Fisher, SJ
在人类妊娠中，侵入子宫的胎盘细胞滋养层下调其上皮来源特征性的粘附受体的表达，并上调由血管细胞表达的粘附受体的表达。我们认为这种转化可能对血管内侵入是至关重要的，细胞滋养层侵入子宫螺旋小动脉并衬在其壁上的过程（Zhou等人，J.Clin.Invest. 1997，99：2139-2151）。为了更好地理解这些发现的体内意义，我们检验了这样的假设，即在先兆子痫中，细胞滋养层不能采用血管粘附表型，在这里描述的实验中，我们对年龄-匹配的对照妊娠和那些患有先兆子痫的妊娠，这些妊娠具有识别粘附分子的抗体，这些粘附分子通常在这种转化过程中被调节。在先兆子痫中，分化/侵入的细胞滋养层不能正确表达许多这些分子，包括整联蛋白、钙粘蛋白和IG超家族成员。这些结果表明先兆子痫与细胞滋养层不能模仿血管粘附表型有关。这种异常的功能后果尚不清楚，但可能会对细胞滋养层血管内浸润和子宫小动脉重塑产生负面影响，从而影响母胎界面的血流。
In human pregnancy, placental cytotrophoblasts that invade the uterus downregulate the expression of adhesion receptors that are characteristic of their epithelial origin, and upregulate the expression of adhesion receptors that are expressed by vascular cells. We suggest that this transformation could be critical to endovascular invasion, the process whereby cytotrophoblasts invade the uterine spiral arterioles and line their walls (Zhou et al. J. Clin. Invest. 1997, 99: 2139-2151.). To better understand the in vivo significance of these findings, we tested the hypothesis that in preeclampsia, an important disease of pregnancy in which endovascular invasion is abrogated, cytotrophoblasts fail to adopt a vascular adhesion phenotype, In experiments described here we stained placental bed biopsy specimens from age-matched control pregnancies and from those complicated by preeclampsia with antibodies that recognize adhesion molecules that are normally modulated during this transformation. In preeclampsia, differentiating/invading cytotrophoblasts fail to express properly many of these molecules, including integrin, cadherin, and Ig superfamily members, These results suggest that preeclampsia is associated with failure of cytotrophoblasts to mimic a vascular adhesion phenotype. The functional consequences of this abnormality are unknown, but are likely to affect negatively cytotrophoblast endovascular invasion and uterine arteriole remodeling, thereby compromising blood flow to the maternal-fetal interface.