FUKUSHIMA Kotaro Kyushu Univ. Hospital, Lecturer, 医学部附属病院, 助手 (40304779)
KOBAYASHI Hiroaki Kyushu Univ. Hospital, Lecturer, 医学部附属病院, 助手 (70260700)
NAKANO Hitoo Graduate School of Medical Sciences, Professor, 大学院・医学研究院, 教授 (40038766)
|Budget Amount *help
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2002: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2001: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2000: ¥1,500,000 (Direct Cost: ¥1,500,000)
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.