Functional differentiation of cytotrophoblast in normal and compromised pregnancies

正常妊娠和受损妊娠中细胞滋养层的功能分化

• 批准号: 12671608
• 负责人: TSUKIMORI Kiyomi
• 金额: $ 1.98万
• 依托单位: Kyushu University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2000
• 资助国家: 日本
• 起止时间: 2000 至 2002
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-12671608/
• 关键词: Preeclampsia; Intrauterine growth restriction; Cytotrophoblast; Endothelial cell; Neutrophil; 子宮内胎児発育遅延; 血管平滑筋細胞; 微小循環動態

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.

为了阐明细胞滋养层细胞（CTB）功能在正常妊娠和受损妊娠中的作用，我们研究了正常妊娠和合并先兆子痫和宫内生长受限（IUGR）妊娠的CTB提取物对体外内皮细胞、中性粒细胞和CTB的每种细胞功能的影响。2）该因子增强嗜中性粒细胞的超氧化物产生，3）由该因子激活的嗜中性粒细胞损伤内皮细胞，以及4）CTB衍生因子刺激CTB中的细胞凋亡。IUGR中存在CTB衍生因子，该因子抑制内皮细胞和CTB的细胞增殖，提示妊娠受损时CTB产生影响内皮细胞、中性粒细胞和CTB各细胞功能的因子。在先兆子痫中，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，以维持胎儿-胎盘-母体微循环的稳态，并且它可能参与先兆子痫临床体征的发展。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，并且其可能与IUGR的病理生理学有关。

项目成果

F.Ushigome, K.Tsukimori et al.: "Human placental transport of vinblastine, vincristine, digoxin and progesterone : contribution of P-glycoprotein"European Journal of Pharmacology. 408. 1-10 (2000)

F.Ushigome、K.Tsukimori 等人：“长春花碱、长春新碱、地高辛和黄体酮的人胎盘转运：P-糖蛋白的贡献”欧洲药理学杂志。

M. Inuyama, K. Tsukimori, et al.: "Characteristics of L-lactic acid transport in basal membrane vesicles of human placental syncytiotrophoblast"American Journal of Physiology Cell Physiology. 283. C822-C830 (2002)

M. Inuyama、K. Tsukimori 等人：“人胎盘合体滋养层基底膜囊泡中 L-乳酸转运的特征”美国生理学细胞生理学杂志。

K.Fukushima, K.Tsukimori et al.: "Cytotoxic Effects of Soluble Factor in Preeclamptic Sera on Human Trophoblasts"American Journal of Reproductive Immunology. 46. 245-251 (2001)

K.Fukushima、K.Tsukimori 等人：“先兆子痫血清中可溶性因子对人类滋养细胞的细胞毒性作用”美国生殖免疫学杂志。

H.Komatsu, K.Tuskimori, et al.: "The characterization of superoxide production of human neonatal neutrophil"Early Human Development. 65. 11-19 (2001)

H.Komatsu、K.Tuskimori 等人：“人类新生儿中性粒细胞超氧化物产生的特征”早期人类发育。

月森清巳, 中野仁雄: "新女性医学大系 妊娠中毒症.病因と病態形成-血管内皮障害-"中山書店. 10 (2001)

Kiyomi Tsukimori、Hiro Nakano：“新女性医学系统先兆子痫。病因学和发病机制 - 血管内皮疾病 -”Nakayama Shoten 10 (2001)。