补体攻膜复合体致肾小球脏层上皮细胞粘附性改变研究

为探讨膜性肾病中补体攻膜复合体(MAC)介导蛋白尿机制,本研究制作了MAC致肾小球脏层上皮细胞(GVEC)亚溶破模型。通过对细胞局部粘附及相关蛋白的观察发现,MAC亚溶破致伤GVEC后,其粘附性发生改变。其机理与ECM分泌失调、膜硫酸化物质及整合素减少、细胞骨架重排有关。这些改变导致体内GVEC脱附,足突退缩融合,从而参与膜性肾病的蛋白尿产生。

EFFECT OF MAC SUBLYTIC INJURY ON FOCAL ADHESION OF CULTURED HUMAN GLOMERULAR VISCERAL EPITHELIAL CELL

It is now well establisbed that proteinuria can be mediated by membrane attack complex of complement (MAC). This mechanism, however ,is not understood. This in vitro study was performed to define the change of focal adhesion and adhesion-associated proteins upon cultured human glomerular visceral epithelial cells (GVEC) to MAC sublytic injury. The results show that this injury brings on imbalance of extracellular matrix protein production,cytoskeleton rearrangement, decrease of integrin and cell surface sulfate proteglycan,with change of GVEC adhesion.which associ-ate with simplification of the foot process,even detachment of GVEC from the GMB,consequent the onset of proteinuria in vivo.