Analysis of serum factor that is related to glomerular hypertrophy and extracellular matrix metabolism.

肾小球肥大及细胞外基质代谢相关血清因子分析

• 批准号: 05670960
• 负责人: MITARAI Tetsuya
• 金额: $ 1.28万
• 依托单位: SAITAMA MEDICAL SCHOOL
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1993
• 资助国家: 日本
• 起止时间: 1993 至 1994
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-05670960/
• 关键词: Mesangial cell; Glomerular hypertrophy; Extra cellular matrix metabolism; Cell matrix interaction; cell-matrix interaction; 培養メサンギウム細胞

It has been well known that glomerular sclerosis and glomerular hypertrophy observe in the remnant kidney after 5/6 nephrectomy. Previous studies indicated that compensatory hypertrophy of the remnant kidney was mediated by serum factor (s), so called renotropic factor. However, it is not clarified whether glomerular hypertrophy is mediated by same factor or not. In the animal experiments, glomerular hypertrophy did not observe when functioning nephron mass were reduced by ureteral diversion. When 5/6 nephrectomy performed using growth hormone deficient rats, glomerular hypertrophy did not observe. In this study, effects of the sera obtained from subtotally nephrectomized animal, in which glomerular sclerosis and glomerular hypertrophy were observed, were evaluated using cultured mesangial cells. The proliferative response evaluated by thymidine uptake were slightly increased by adding the nephrectomized serum, especially in the fraction of MW less than 3000. Concerning about the extra cellular matrix metabolism evaluated by northern blot analysis, there were no obvious effects in the sera. Cell-matrix interactions were studied by using gel contraction method, and the sera from 5/6 nephrectomized mice increased gel contraction. In conclusion, some factors that affect mesangial cell behavior present in the serum obtained from 5/6 nephrectomized animal in which glomerular hypertrophy observe. However it was not able to demonstrate the effects of the sera to extra cellular matrix metabolism.

众所周知，5/6肾切除术后残肾可出现肾小球硬化和肥大。以往的研究表明，残肾代偿性肥大是由血清促肾因子介导的。然而，肾小球肥大是否由同一因子介导尚不清楚。在动物实验中，当输尿管转流减少功能性肾单位质量时，未观察到肾小球肥大。当使用生长激素缺乏大鼠进行5/6肾切除时，未观察到肾小球肥大。在这项研究中，使用培养的系膜细胞评价了从肾部分切除动物中获得的血清的作用，其中观察到肾小球硬化和肾小球肥大。通过胸苷摄取评估的增殖反应通过加入肾切除血清而略微增加，尤其是在MW小于3000的部分中。用北方印迹法检测细胞外基质代谢，对血清无明显影响。用凝胶收缩法研究细胞-基质相互作用，5/6肾切除小鼠血清可增加凝胶收缩。结论：5/6肾切除大鼠血清中存在影响系膜细胞行为的因素。然而，它不能证明血清对细胞外基质代谢的影响。

项目成果

Yoshida, H, Mitarai, T, 他: "The effect of selective growth hormone defect in progression of glomerulosclerosis" Am J Kidney Dis. 23. 302-312 (1994)

Yoshida, H, Mitarai, T 等人：“选择性生长激素缺陷对肾小球硬化症进展的影响”Am J Kidney Dis. 23. 302-312 (1994)

Yoshida H,Mitarai T,Kitamura M,Suzuki T,Ishikawa H,Fogo A,Sakai O.: "The effect of selective growth hormone defect in progression of glomwrulosclerosis." Am J Kidney Dis.23. 302-312 (1994)

Yoshida H、Mitarai T、Kitamura M、Suzuki T、Ishikawa H、Fogo A、Sakai O.：“选择性生长激素缺陷对肾小球硬化症进展的影响。”