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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。
In order to investigate the mechanism of complement-omembranous membrane complex (MAC) -mediated proteinuria in membranous nephropathy, a MAC-induced subarachitic model of glomerular visceral epithelial cells (GVEC) was made in this study. Through the observation of local adhesion of cells and related proteins, it was found that the adhesion of GVEC was changed after MAC subfusions broke GVEC. The mechanism of ECM secretion disorders, membrane sulfation substances and integrins decreased cytoskeletal rearrangement. These changes lead to the in vivo GVEC desorption, foot process retreat fusion, and thus participate in the proteinuria of membranous nephropathy.