Accelerated wound healing in leukocyte-specific, protein 1-deficient mouse is associated with increased infiltration of leukocytes and fibrocytes

Autor: Paul G. Scott, Megan V. H. Lyons, Heather A. Shankowsky, Tara L. Stewart, Haiyan Jiao, Edward E. Tredget, JianFei Wang
Rok vydání: 2007
Předmět:
Zdroj: Journal of Leukocyte Biology. 82:1554-1563
ISSN: 1938-3673
0741-5400
DOI: 10.1189/jlb.0507306
Popis: Wound healing is a complex process involving the integrated actions of numerous cell types, soluble mediators, and ECM. Recently, a newly identified cell type, the fibrocyte, has been reported to contribute to wound healing and fi- brotic conditions such as hypertrophic scarring. We previously established leukocyte-specific pro- tein 1 (LSP1) as a marker for fibrocytes. LSP1 is an F-actin binding protein and substrate of p38 mitogen-activated protein kinase and protein ki- nase C, and has been reported to be important in leukocyte chemotaxis. We examine the biological roles of LSP1 in skin wound healing using Lsp1 / null mice. These animals showed accelerated heal- ing of full-thickness skin wounds, with increased re-epithelialization rates, collagen synthesis, and angiogenesis. Healing wounds in Lsp1 / mice had higher densities of neutrophiles, macrophages, and fibrocytes. Along with increased leukocyte infiltra- tion, levels of macrophage-derived chemokine ex- pression, TGF-1, and VEGF were all up-regu- lated. These results demonstrate that the absence of LSP1 promotes healing of skin wounds. The primary mechanism seems to be an increase in leukocyte infiltration, leading to locally elevated synthesis and release of chemokines and growth factors. Further analysis of Lsp1 / mice may sug- gest ways to improve wound healing and/or treat fibrotic conditions of skin and other tissue. J. Leu- koc. Biol. J. Leukoc. Biol. 82: 1554-1563; 2007.
Databáze: OpenAIRE
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