Trophoblast deportation in human pregnancy - its relevance for pre-eclampsia
Trophoblast deportation in human pregnancy - its relevance for pre-eclampsia
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DOI：
10.1053/plac.1999.0422
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发表时间：
1999-09-01
期刊：
影响因子：
3.8
通讯作者：
Sargent, IL
中科院分区：
文献类型：
--
作者：
Johansen, M;Redman, CWG;Sargent, IL
先兆子痫的母体综合征被认为是由来自胎盘的循环因子引起的内皮细胞损伤引起的。本研究调查的假设，滋养层驱逐可能是这个因素进入母体循环的过程的一部分。研究了正常和先兆子痫妇女剖宫产时子宫静脉和外周血中滋养细胞排出的性质和发生率。滋养层细胞富集使用免疫磁珠消耗白细胞和标记与滋养层细胞特异性单克隆抗体。子宫静脉血中可见合体滋养细胞、细胞滋养细胞、细胞滋养细胞团和无核滋养细胞。细胞滋养层细胞脱落的频率低于合体滋养层细胞，大多数可能是绒毛起源。正常孕妇子宫静脉血中存在滋养层细胞，子痫前期孕妇的滋养层细胞水平较高。然而，滋养细胞很少发现在外周循环。滋养层细胞数量与疾病的严重程度、胎盘病理的程度或子宫和外周静脉血浆对体外内皮生长的抑制作用之间没有相关性。因此，据推测，先兆子痫中滋养层驱逐增加是继发于胎盘中发生的结构和功能变化，而不是与先兆子痫中的循环内皮细胞损伤因子直接相关。(C)1999年哈考特出版社有限公司
The maternal syndrome of pre-eclampsia is thought to result from endothelial cell damage caused by a circulating factor derived from the placenta. This study investigates the hypothesis that trophoblast deportation may be part of the process by which this factor enters the maternal circulation. The nature and incidence of trophoblast deportation was studied in uterine vein and peripheral blood taken from normal and pre-eclamptic women at caesarean section. Trophoblasts were enriched using immunomagnetic beads to deplete leucocytes and labelled with trophoblast-specific monoclonal antibodies. Syncytiotrophoblast, cytotrophoblast, cytotrophoblast clumps and anucleate trophoblast cells were found in uterine vein blood. Cytotrophoblast cells were found to be shed less frequently than syncytiotrophoblast and the majority were probably villous in origin. Trophoblasts were found in the uterine vein blood of normal pregnant women with higher levels in pre-eclampsia. However, trophoblasts were rarely found in the peripheral circulation. There was no correlation between trophoblast numbers and either the severity of the disease, the extent of placental pathology or the inhibitory effect of uterine and peripheral vein plasma on endothelial growth in vitro. Thus, it is speculated that increased trophoblast deportation in pre-eclampsia is secondary to the structural and functional changes occurring in the placenta, rather than directly linked with the circulating endothelial cell damaging factor in pre-eclampsia. (C) 1999 Harcourt Publishers Ltd.