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Am J Physiol Cell Physiol (January 14, 2004). doi:10.1152/ajpcell.00467.2003
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Submitted on October 24, 2003
Accepted on January 12, 2004

The Role of C-C Chemokines in Skeletal Muscle Functional Restoration Post-Injury

Gordon L Warren1, Laura O'Farrell1, Mukesh Summan2, Tracy Hulderman2, Dawn Mishra2, Michael I Luster2, William A Kuziel3, and Petia P Simeonova2*

1 Department of Physical Therapy, Georgia State University, Atlanta, GA, USA
2 HELD, TMBB, NIOSH, CDC, Morgantown, WV, USA
3 Molecular Genetics, University of Texas, Austin, TX, USA

* To whom correspondence should be addressed. E-mail: PSimeonova{at}cdc.gov.

The purpose of this study was to determine whether certain chemokines, which are highly expressed in injured skeletal muscle, are involved in the repair and functional recovery of the muscle after traumatic injury. In wild-type control mice, mRNA transcripts of macrophage-inflammatory protein (MIP)-1{alpha}, MIP-1{beta}, and monocyte chemoattractant protein (MCP)-1 as well as of their major receptors, CCR5 and CCR2, increased following freeze injury and gradually returned to control (uninjured) levels by 14 days. Muscle function and histological characteristics were monitored in injured mice that were genetically deficient for the CCR5 receptor (a major receptor for MIP-1{alpha} and MIP-1{beta}) and also rendered MCP-1 deficient with neutralizing antibodies. To dissect the role of these chemokines, additional studies were conducted in CCR5- and CCR2-deficient mice. CCR5-/- mice injected with MCP-1 antiserum for the first 3 days post-injury exhibited a 2-fold greater maximal isometric tetanic torque deficit at 14 days post-injury than did controls (i.e., 33% vs. 17%; p = 0.002). The impaired functional recovery was accompanied with an increased fat infiltration within the regenerating muscle without a significant difference in the influx of inflammatory cells, including macrophages. Strength recovery was also impaired in mice deficient for the receptor of MCP-1, CCR2, but not in CCR5-/- mice that were not injected with MCP-1-antiserum. The data suggests that MCP-1/CCR2 plays a role in the regeneration and recovery of function after traumatic muscle injury.




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