Functional differentiation of cytotrophoblast in normal and compromised pregnancies

为了明确细胞滋养细胞（CTB）功能在正常妊娠和受损妊娠中的作用，我们在体外研究了正常妊娠和合并子痫前期和宫内生长受限（IUGR）妊娠的细胞滋养细胞提取物对内皮细胞、中性粒细胞和CTB各细胞功能的影响。在子痫前期，可以明确1)CTB衍生因子对内皮细胞有细胞毒性，2)该因子增强超氧化物中性粒细胞的产生，3)该因子激活的中性粒细胞损伤内皮细胞，4)CTB衍生因子刺激CTB细胞凋亡。在IUGR中，可以明确存在一种CTB衍生因子，它可以抑制内皮细胞和CTB的细胞增殖。综上所述，CTB在妊娠受损时产生影响内皮细胞、中性粒细胞和CTB各细胞功能的因子。在子痫前期，ctb衍生因子涉及细胞间相互作用失败，特别是发生在内皮细胞和中性粒细胞之间，以维持胎-胎盘-母体微循环的稳态，它可能参与子痫前期临床症状的发展。在IUGR中，CTB衍生因子参与胎盘发育，抑制内皮细胞和CTB的细胞增殖，可能与IUGR的病理生理有关。

To clarify the role of cytotrophoblast (CTB) function in normal and compromised pregnancies, we investigated the effect of CTB extract from normal pregnancy and those complicated with preeclampsia and intrauterine growth restriction (IUGR) on each cell function of endothelial cell, neutrophil and CTB in vitro.In preeclampsia, it is cleared that 1) a CTB-derived factor cytotoxic to endothelial cells is present, 2) This factor enhances superoxide production of neutrophils, 3) Activated neutrophils by this factor injure endothelial cells, and 4) A CTB-derived factor stimulates apoptosis in CTB. In IUGR, it is cleared that a CTB-derived factor, which inhibits cellular proliferation of both endothelial cells and CTB, is present.From the above findings, it is suggested that CTB produce factors, which affect on each cell function of endothelial cell, neutrophil and CTB, in compromised pregnancies. In preeclampsia, a CTB-derived factor involves cell-to-cell interaction failure, particularly occurring between the endothelium and neutrophils, to maintain homeostasis of feto-placental-maternal microcirculation, and it might participate in development of clinical sign of preeclampsia. In IUGR, a CTB-derived factor involves placental development, to inhibit cellular proliferation of both endothelial cells and CTB, and it might relate to the pathophysiology of IUGR.