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

Zinostatin stiMalamer(ZS)诱导的肾小球损伤是由系膜细胞内皮细胞肿胀、内皮下间隙扩张，伴随着血管内皮生长因子的大量表达而引起的。巨噬细胞聚集在损伤的肾小球内，随后系膜细胞表型转化，肾小球内III型和IV型胶原积聚。免疫组织化学和RT-PCR研究表明，肾小球内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内细胞外基质积聚。根据肾小球病变的不同阶段，转化生长因子-β1、2和3的表达有不同的定位。

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.