Glomerular expression of monocyte chemoattractant protein-1 in experimental and human glomerulonephritis.

Glomerular expression of monocyte chemoattractant protein-1 in experimental and human glomerulonephritis.
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发表时间:
1994-10
期刊:
Laboratory investigation; a journal of technical methods and pathology
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通讯作者:
Rovin Bh;M. Rumancik;L. Tan;J. Dickerson
Rovin Bh;M. Rumancik;L. Tan;J. Dickerson
中科院分区:
其他
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作者:
Rovin Bh;M. Rumancik;L. Tan;J. Dickerson

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肾小球单核细胞存在于多种肾脏疾病中,在肾小球损伤的发病机制中起重要作用。负责募集单核细胞到肾小球的介质没有很好的特点。我们最近已经确定,培养的人肾小球系膜细胞产生特异性的单核细胞趋化蛋白,单核细胞趋化蛋白-1(MCP-1)在肾小球肾炎(GN)过程中,在肾小球中常见的炎症细胞因子的反应。这表明MCP-1可能参与了白细胞向肾小球的募集。然而,迄今为止,关于MCP-1在肾脏疾病期间的表达的信息很少。本研究旨在研究MCP-1在实验性和人类GN中的体内表达。实验设计采用抗肾小球基底膜肾炎的啮齿动物模型,研究肾小球MCP-1 mRNA调控和蛋白表达。MCP-1在人肾组织中的存在通过免疫染色来自患有各种肾小球病的患者的肾活检材料来研究。结果MCP-1 mRNA在实验性肾小球肾炎早期即有短暂的上调。消息水平增加与单核细胞流入和相关的免疫反应性MCP-1在肾炎肾小球的表达。在人类炎症性肾小球病中也发现了肾小球MCP-1,但在缺乏显著单核细胞浸润的肾小球疾病中未发现。结论:这些数据支持MCP-1在肾小球炎症发病机制中的作用。
BACKGROUND Glomerular monocytes are found in a variety of renal diseases and appear to be important in the pathogenesis of glomerular injury. The mediators responsible for recruiting monocytes to the glomerulus are not well characterized. We have recently established that cultured human mesangial cells produce the specific monocyte chemoattractant, monocyte chemoattractant protein-1 (MCP-1) in response to inflammatory cytokines commonly found in glomeruli during glomerulonephritis (GN). This suggested that MCP-1 may be involved in recruiting leukocytes to the glomerulus. To date however, there is little information regarding the expression of MCP-1 during renal disease. The present study was undertaken to investigate the in vivo expression of MCP-1 during experimental and human GN. EXPERIMENTAL DESIGN A rodent model of anti-glomerular basement membrane GN was used to investigate glomerular MCP-1 mRNA regulation and protein expression. The presence of MCP-1 in human renal tissue was studied by immunostaining kidney biopsy material from patients with a variety of glomerulopathies. RESULTS MCP-1 mRNA was transiently upregulated during the early stages of experimental GN. Message levels increased in association with the monocyte influx and correlated with expression of immunoreactive MCP-1 in the nephritic glomeruli. Glomerular MCP-1 was also found in human inflammatory glomerulopathies, but not in glomerular diseases lacking a prominent monocyte infiltrate. CONCLUSIONS These data support a role for MCP-1 in the pathogenesis of glomerular inflammation.