Low, QEH, Drugea, IA, Duffner, LA, Quinn, Daniel, Cook, DN, Rollins, BJ, Kovacs, EJ and DiPietro, LA (2001) Wound healing in MIP-1 alpha(-/-) and MCP-1(-/-) mice. AMERICAN JOURNAL OF PATHOLOGY, 159 (2). pp. 457-463. [Journal article]
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A salient feature of normal wound healing is the development and resolution of an acute inflammatory response. Although much is known about the function of inflammatory cells within wounds, little is known about the chemotactic and activation signals that influence this response. As the CC chemokines macrophage inflammatory protein-1 alpha (MEP-1 alpha) and monocyte chemotactic protein-1 (MCP-1) are abundant in acute wounds, wound repair was examined in MIP-1 alpha (-/-) and MCP-1(-/-) mice. Surprisingly, wound re-epithelialization, angiogenesis, and collagen synthesis in MIP-1 alpha (-/-) mice was nearly identical to wildtype controls. In contrast, MCP-1(-/-) mice displayed significantly delayed wound re-epithelialization, with the greatest delay at day 3 after injury (28 +/- 5% versus 79 +/- 14% re-epithelialization, P < 0.005). Wound angiogenesis was also delayed in MCP-1(-/-) mice, with a 48% reduction in capillary density at day 5 after injury. Collagen synthesis was impeded as well, with the wounds of MCP-1(-/-) mice containing significantly less hydroxyproline than those of control mice (25 <plus/minus> 3 versus 50 +/- 8 mug/wound at day 5, P < 0.0001). No change in the number of wound macrophages was observed in MCP-1(-/-) mice, suggesting that monocyte recruitment into wounds is independent of this chemokine. The data suggest that MCP-1 plays a critical role in healing wounds, most likely by influencing the effector state of macrophages and other cell types.
|Item Type:||Journal article|
|Faculties and Schools:||Faculty of Life and Health Sciences > School of Biomedical Sciences|
Faculty of Life and Health Sciences
|Deposited By:||Dr Daniel Quinn|
|Deposited On:||31 Jul 2012 09:27|
|Last Modified:||31 Jul 2012 09:27|
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