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This Article Full Text Full Text (PDF) All Versions of this Article: 293/3/R1152    most recent 00132.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Bryer, S. C. Articles by Koh, T. J. Search for Related Content PubMed PubMed Citation Articles by Bryer, S. C. Articles by Koh, T. J.

INFLAMMATION AND CYTOKINES

The urokinase-type plasminogen activator receptor is not required for skeletal muscle inflammation or regeneration

Department of Movement Sciences, University of Illinois at Chicago, Chicago, Illinois

Submitted 16 April 2007 ; accepted in final form 11 June 2007

The hypothesis of this study was the urokinase-type plasminogen activator receptor (uPAR) is required for accumulation of inflammatory cells in injured skeletal muscle and for efficient muscle regeneration. Expression of uPAR was elevated at 1 and 3 days after cardiotoxin-induced muscle injury in wild-type mice before returning to baseline levels. Neutrophil accumulation peaked 1 day postinjury in muscle from both wild-type (WT) and uPAR null mice, while macrophage accumulation peaked between 3 and 5 days postinjury, with no differences between strains. Histological analyses confirmed efficient muscle regeneration in both wild-type and uPAR null mice, with no difference between strains in the formation or growth of regenerating fibers, or recovery of normal morphology. Furthermore, in vitro experiments demonstrated that chemotaxis is not different between WT and uPAR null macrophages. Finally, fusion of cultured satellite cells into multinucleated myotubes was not different between cells isolated from WT and uPAR null mice. These results demonstrate that uPAR is not required for the accumulation of inflammatory cells or the regeneration of skeletal muscle following injury, suggesting uPA can act independently of uPAR to regulate events critical for muscle regeneration.

muscle repair; macrophage; chemotaxis

This article has been cited by other articles:

				M. Cheng, M.-H. Nguyen, G. Fantuzzi, and T. J. Koh Endogenous interferon-{gamma} is required for efficient skeletal muscle regeneration Am J Physiol Cell Physiol, May 1, 2008; 294(5): C1183 - C1191. [Abstract] [Full Text] [PDF]