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1 Toxicology and Molecular Biology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV, USA
2 Department of Physical Therapy, Georgia State University, Atlanta, GA, USA
3 Department of Molecular Cell Biology, Vrije University, Amsterdam, Netherlands, none
* To whom correspondence should be addressed. E-mail: PSimeonova{at}cdc.gov.
The study evaluates the influence of monocytes/macrophages in the mechanisms of skeletal muscle injury using a mouse model and selective depletion of peripheral monocyte with systemic injections of liposomal clodronate (dichloromethylene bisphosphonate). This pharmacological treatment has been demonstrated to induce specific apoptotic death in monocytes and phagocytic macrophages. In the current studies, the liposomal clodronate injections resulted in a marked attenuation of the peak inflammatory response in the freeze-injured muscle in the first three days after injury. The effect was accompanied by a transient reduction (at day 1 or 3 post-injury) of the expression of several genes coding for inflammatory as well as growth-related mediators including tumor necrosis factor (TNF), monocyte chemoattractant protein (MCP)-1, thioredoxin, high mobility group AT-hook 1, insulin-like growth factor-binding protein (IGFBP), and IGF-1. In contrast, the expression of major myogenic factors (i.e., MyoD and myogenin) directly involved in the activation/proliferation and differentiation of muscle precursor cells was not altered by the clodronate-liposome treatment. The repair process in the injured muscle of clodronate-liposome treated mice was characterized with prolonged clearance of necrotic myofibers and a tendency for increased muscle fat accumulation at day 9 and 14 post injury, respectively. In conclusion, a significant reduction of the initial monocyte/macrophage influx into the injured muscle is associated with not improved but moderately impaired repair processes following skeletal muscle injury.
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