足细胞
肾小球硬化
血小板源性生长因子受体
医学
发病机制
内科学
肾功能
肾小球肾炎
内分泌学
苏帕
血小板衍生生长因子
生长因子
肾
蛋白尿
受体
尿激酶受体
作者
Tammo Ostendorf,Uta Kunter,H. J. Gröne,Ferdinand H. Bahlmann,Hiroshi Kawachi,Fujio Shimizu,K. M. Koch,Nebojša Janjić,Jürgen Floege
出处
期刊:Journal of The American Society of Nephrology
日期:2001-05-01
卷期号:12 (5): 909-918
被引量:121
摘要
Abstract. Glomerular mesangial cell proliferation and/or mesangial matrix accumulation characterizes many progressive renal diseases. Rats with progressive mesangioproliferative glomerulonephritis were treated from day 3 to day 7 after disease induction with a high-affinity oligonucleotide aptamerantagonist against platelet-derived growth factor-B chain (PDGF-B). In comparison with nephritic rats that received vehicle or a scrambled aptamer, treatment with the PDGF-B aptamer led to a significant reduction of mesangioproliferative changes, glomerular hypertrophy, podocyte damage, and glomerular macrophage influx on day 8. Both nephritic control groups subsequently developed progressive proteinuria and decreased renal function. On day 100, glomerulosclerosis, tubulointerstitial damage, glomerular and interstitial accumulation of types III and IV collagen, and overexpression of transforming growth factor-β were widespread. All of these chronic changes were prevented in rats that received the PDGF-B aptamer, and their functional and morphologic parameters on day 100 were largely indistinguishable from non-nephritic rats. These data provide the first evidence for a causal role of PDGF in the pathogenesis of renal scarring and point to a new, highly effective therapeutic approach to progressive, in particular mesangioproliferative, renal disease.
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