Nephrol Dial Transplant (1999) 14: 2554-2556
© 1999 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
The proinflammatory role of hyaluronan–CD44 interactions in renal injury
Division of Nephrology, Department of Medicine, University Hospital and Physiological Institute, University Zürich-Irchel, Switzerland
Correspondence and offprint requests to: Rudolf P. Wüthrich, Division of Nephrology, Department of Medicine, University Hospital, Rämistrasse 100, CH-8091 Zurich, Switzerland.
Introduction
Numerous proinflammatory pathways that lead to mononuclear leukocyte invasion have been described in renal disease. These include upregulation of cytokines with ensuing activation of adhesion molecules, stimulation of chemokines with subsequent chemotaxis, and activation of the complement and coagulation cascades that promote leukocyte activation. Recently, we have shown that the enhanced accumulation of the matrix molecule hyaluronan (HA) in the cortical renal interstitium is linked to these classical proinflammatory events in the kidney. Here we discuss the consequences resulting from the interaction of HA with its specific cell surface receptor CD44 on renal parenchymal cells.
Hyaluronan synthesis and degradation in the kidney
HA is an important component of the extracellular matrix. It is composed of endless linear repeats of the disaccharide unit (N-acetyl-D-glucosamine [ß1
4] D-glucuronic acid [ß13]) [1,2]. HA is synthesized by specific HA synthases (HAS) and is extruded into the extracellular
The hyaluronan-receptor CD44 is upregulated in inflammatory renal diseases
Proinflammatory effects of hyaluronan fragments in renal cells
Can the HA/CD44 pathway be influenced by therapeutic manoeuvres?
Acknowledgments
References
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