Johansen M, Redman C W, Wilkins T, Sargent I L
Nuffield Department of Obstetrics and Gynaecology, University of Oxford, John Radcliffe Hospital, Oxford, OX3 9DU, UK.
Placenta. 1999 Sep;20(7):531-9. doi: 10.1053/plac.1999.0422.
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.
子痫前期的母体综合征被认为是由胎盘来源的循环因子导致的内皮细胞损伤所致。本研究调查了一个假说，即滋养层细胞脱落可能是该因子进入母体循环过程的一部分。在剖宫产时从正常孕妇和子痫前期孕妇采集的子宫静脉血和外周血中，研究了滋养层细胞脱落的性质和发生率。使用免疫磁珠富集滋养层细胞以去除白细胞，并用滋养层特异性单克隆抗体进行标记。在子宫静脉血中发现了合体滋养层细胞、细胞滋养层细胞、细胞滋养层细胞团和无核滋养层细胞。发现细胞滋养层细胞的脱落频率低于合体滋养层细胞，且大多数可能起源于绒毛。在正常孕妇的子宫静脉血中发现了滋养层细胞，子痫前期患者的水平更高。然而，在外周循环中很少发现滋养层细胞。滋养层细胞数量与疾病严重程度、胎盘病理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均无相关性。因此，推测子痫前期滋养层细胞脱落增加是胎盘发生的结构和功能变化的继发结果，而非直接与子痫前期循环中的内皮细胞损伤因子相关。
