Traumatic skeletal muscle injury causes a specific sequence of cellular events consisting of degeneration, inflammation, regeneration, and fibrosis. The role of early posttraumatic mechanisms, including acute inflammatory response, in muscle repair is not well understood. In the present study, oligonucleotide microarray analyses were used to examine the candidate genes that are involved in these early events of the muscle injury/repair process. cDNA was prepared from the injured and control tibialis anterior (TA) muscle of mice 24 h postinjury and labeled with the fluorescent dye Cy5 or Cy3 prior to hybridization to a DNA microarray. The microarray analysis, including 732 genes, was conducted in triplicate, and we describe only genes modulated by the injury showing a differential expression (both increased and decreased) 1.7-fold or greater (p < 0.05) from control uninjured TA muscle. Selected expression patterns were confirmed by other gene expression detection methods, including real-time reverse transcription-polymerase chain reaction (RT-PCR) and RNase protection assay (RPA) or immunohistochemistry detection methods. The upregulated genes (2.8%) were mainly associated with inflammation, oxidative stress, and cell proliferation, whereas the downregulated genes (3.2%) were related to metabolic and cell signaling pathways. In addition, the study suggested that chemokines, such as monocyte chemoattractant protein-1 (MCP-1), associated with monocyte/macrophage influx and activation, are abundantly expressed in postinjured muscle, and they might play a role in traumatic muscle injury/recovery processes.
Toxicology & Molecular Biology Branch, National Institute for Occupational Safety and Health, Morgantown, WV 26505-2888