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Effects of maternal chronic uremia on the development of fetal kidney : expression of growth factors and genes

母亲慢性尿毒症对胎儿肾脏发育的影响：生长因子和基因的表达

基本信息

批准号：
10660288
负责人：
OKADA Toshiya
金额：
$ 2.18万
依托单位：
Osaka Prefecture University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 2000
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10660288/
关键词：
maternal nephrectomy fetal kidney cell proliferation apoptosis growth factor oncogene tumor suppressor gene apoptosis suppressor gene p53 WT1 EGFR 胎児腎臓 insulin like growth factor1 epidermal growth factor receptor proliferating

项目摘要

The present study designed to clarify the development of fetal kidney when maternal kidney become dysfunctional. During perinatal period, intense cell proliferation and apoptosis were present in the kidney. The number of proliferating cells was decreased with age at this period. Percentage of apoptotic cells in fetal kidney was significantly increased from fetal day 18 through 20 and decreased thereafter. Maternal uninephrectomy induced lowered proliferative activity of mature glomerulus, increased immunoreactivity of vascular endothelial growth factor (VEGF) of immature glomerulus and increased immunoreactivities of epidermal growth factor (EGF) and EGF receptor in proximal tubules in fetal kidney. Further, maternal uninephrectomy induced increased number of apoptotic cells of collecting ducts and decreased expressions of c-fos, bcl-2, p53 and WT 1 mRNA.These results indicate that the development of fetal kidney is accelerated by maternal uninephrectomy, that the lowered proliferative activity of mature glomerulus is due to the enhanced expression of VEGF in immature glomerulus and decreased expression of oncogene (c-fos), and that the increase of apoptosis in collecting ducts is due not to elevated expression of tumor suppressor gene but to decreased expression of apoptosis suppressor gene.

本研究旨在阐明母体肾脏功能障碍时胎儿肾脏的发育。在围产期，肾脏中存在着强烈的细胞增殖和凋亡。增殖细胞数随年龄增长而减少。胎肾中凋亡细胞百分比在胎龄18 ~ 20天显著增加，此后下降。孕鼠单侧肾切除后，成熟肾小球增殖活性降低，未成熟肾小球血管内皮生长因子（VEGF）免疫反应性增强，胎儿近端小管表皮生长因子（EGF）及其受体免疫反应性增强。孕鼠单肾切除后，集合管凋亡细胞增多，c-fos、bcl-2、p53和WT 1 mRNA表达降低，提示孕鼠单肾切除促进了胎肾的发育，成熟肾小球增殖活性降低是由于未成熟肾小球VEGF表达增强和癌基因c-fos表达降低所致。集合管细胞凋亡的增加不是由于抑癌基因的表达增加，而是由于凋亡抑制基因的表达减少。