Nephrol Dial Transplant (2002) 17: 2043-2047
© 2002 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
Monocyte chemoattractant protein-1 (MCP-1) in the kidney: does it more than simply attract monocytes?
1 Department of Internal Medicine, Division of Cardiology, Ruperto Carola University, Heidelberg, Germany and 2 Division of Nephrology and Hypertension, University Hospital of Berne (Inselspital), Switzerland
Keywords: activator protein-1; intercellular adhesion molecule-1; interleukin-6; monocyte chemoattractant protein-1; nuclear factor-
B; tubular epithelial cells
| The first 150 words of the full text of this article appear below. |
MCP-1: a player in the pathogenesis of progression of renal diseases
There is an increasing body of evidence that the CC chemokine monocyte chemoattractant protein-1 (MCP-1) plays a major role in the pathogenesis of progression of renal failure. This is based on observations both in various animal models of renal damage and in different types of human renal disease (for review, see [1]). Locally produced MCP-1 seems to be particularly involved in the initiation and progression of tubulointerstitial damage. The latter has been documented in experiments using transgenic mice with nephrotic serum-induced nephritis: compared with wild-type mice, MCP-1-deficient mice exhibit less tubulointerstitial lesions, but they exhibit no differences in glomerular lesions [2]. There is, however, evidence that MCP-1 also plays a role in the progression of glomerular lesions, since glomerular expression of MCP-1 correlates with the degree of renal damage in inflammatory [3] and non-inflammatory [4] models of glomerular injury. Furthermore, in humans
MCP-1 induces an inflammatory activation of human tubular epithelial cells
Which receptor(s) is responsible for the mediation of effects of MCP-1 on human tubular epithelial cells?
Conclusion
Note added in proof
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