溶解体损伤不激活nf - κ B,也不诱导大鼠系膜细胞有丝分裂。

S J Mudge, J L McRae, R B Auwardt, B F Murphy, C G Chen, D A Power
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引用次数: 4

摘要

补体末端膜攻击复合物(C5b-9)介导的肾小球系膜细胞的溶解体损伤是IgA肾病的潜在启动机制。据报道,补体亚溶损伤导致多种促炎分子和生长因子的产生,包括许多由转录因子NF-kappa B调节的因子。为了确定补体损伤在IgA肾病中发生的促炎信号传导中的重要性,我们研究了培养大鼠肾小球系膜细胞(RMCs)的补体亚溶损伤后NF-kappa B的激活。通过流式细胞术、铬释放试验和诱导超氧化物产生的方法,选择兔抗THY 1.1 (THY)血清和正常人血清亚溶剂量。电泳迁移量转移试验、转染NF-kappa B驱动的荧光素酶报告结构的RMCs的荧光素酶活性、NF-kappa B响应的mRNA物种单核细胞化学引诱蛋白-1或I -kappa B α的Northern印迹检测均未检测到c5b -9诱导的NF-kappa B活化。此外,与热灭活血清治疗和单独使用THY相比,亚溶补体损伤后(3)H掺入的测量显示,系膜细胞有丝分裂发生受到抑制。本研究结果提示,亚溶补体损伤RMC并不直接激活NF-kappa B,也不诱导系膜细胞的增殖。其他机制,如IgA免疫复合物的形成,必须在IgA肾病中产生这些事件。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sublytic complement injury does not activate NF-kappa B, or induce mitogenesis in rat mesangial cells.

Sublytic complement injury to glomerular mesangial cells, mediated by the terminal membrane attack complex of complement (C5b-9), is a potential initiating mechanism in IgA nephropathy. Sublytic complement injury has been reported to result in the production of a variety of pro-inflammatory molecules and growth factors, including many regulated by the transcription factor NF-kappa B. To determine the importance of complement injury in the pro-inflammatory signalling which occurs in IgA nephropathy, we investigated NF-kappa B activation following sublytic complement injury to cultured rat glomerular mesangial cells (RMCs). A sublytic dose of rabbit anti-Thy 1.1 (THY) serum and normal human serum was selected based upon flow cytometry, chromium-release assay, and induction of superoxide production. No significant C5b-9-induced NF-kappa B activation was detected by electrophoretic mobility shift assays, luciferase activity of RMCs transfected with a NF-kappa B-driven luciferase reporter construct, nor by Northern blots for the NF-kappa B-responsive mRNA species monocyte chemoattractant protein-1 or I kappa B alpha. Furthermore, measurements of (3)H incorporation following sublytic complement injury showed inhibition of mesangial cell mitogenesis in comparison to the heat-inactivated serum treatment and to THY alone. The results of this study suggest that sublytic complement injury to RMC does not directly activate NF-kappa B nor induce mesangial cell proliferation in mesangial cells. Other mechanisms such as IgA immune complex formation must be required to produce these events in IgA nephropathy.

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