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From the Departments of Surgery,
*
Medicine,
and Physiology and Cellular
Biophysics,
College of Physicians &
Surgeons, Columbia University, New York, New York
Receptor for advanced glycation end-products (RAGE),
and two of its ligands, AGE and EN-RAGEs (members of the
S100/calgranulin family of pro-inflammatory cytokines), display
enhanced expression in slowly resolving full-thickness excisional
wounds developed in genetically diabetic db+/db+ mice. We tested the
concept that blockade of RAGE, using soluble(s) RAGE,
the extracellular ligand-binding domain of the receptor, would
enhance wound closure in these animals. Administration of sRAGE
accelerated the development of appropriately limited inflammatory cell
infiltration and activation in wound foci. In parallel with accelerated
wound closure at later times, blockade of RAGE suppressed
levels of cytokines; tumor necrosis factor-
; interleukin-6; and
matrix metalloproteinases-2, -3, and -9. In
addition, generation of thick, well-vascularized
granulation tissue was enhanced, in parallel with increased
levels of platelet-derived growth factor-B and vascular endothelial
growth factor. These findings identify a central role for RAGE in
disordered wound healing associated with diabetes, and suggest
that blockade of this receptor might represent a targeted strategy to
restore effective wound repair in this disorder.
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