Study on changes of extra-cellular matrix in chemical-induced renal glomerular injury

化学性肾小球损伤中细胞外基质变化的研究

• 批准号: 09660346
• 负责人: SHIROTA Kinji
• 金额: $ 2.18万
• 依托单位: AZABU UNIVERCITY
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1997
• 资助国家: 日本
• 起止时间: 1997 至 1999
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09660346/
• 关键词: KIDNEY; CYTOKINE; EXTRA-CELLULAR MATRIX; 糸球体硬化

The golmerular injury induced by Zinostatin stimalamaer(ZS) is initiated by endothelial swelling, dilatation of subendothelial spaces associated with expression of VEGF in the mesangial cells followed by massive influx of macromolecules in to the mesangiaum from the capillary lumen.The macrophages accumulate in the injured glomeruli followed by phenotypic transformation of mesangial cells and accumulation of types-III and IV collage in the glomeruli.Immunohistochemical and RT-PCR studies suggested that infiltrated macrophages and glomerular cells produced IL-1, IL-6 followed by extra-cellular matrix accumulation in the injured glomeruli.The expression of TGF-beta isoforms 1, 2 and 3 is different in localization depending on the stages of this glomerulopathy.

由Zinostatin stimalamaer（ZS）诱导的肾小球损伤由内皮肿胀起始，肾小球系膜细胞中VEGF表达导致内皮下空间扩张，随后大分子物质从毛细血管腔大量流入系膜。巨噬细胞在受损肾小球中积聚，随后系膜细胞表型转化，免疫组织化学和RT-PCR研究表明，浸润的巨噬细胞和肾小球细胞产生IL-1，IL-6，随后在损伤的肾小球中细胞外基质积累。2和3在定位上是不同的，这取决于该肾小球病的阶段。