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Updated: Sep 25, 2026
Identification and Analysis of Myogenic Progenitors In Vivo During Acute Skeletal Muscle Injury by High-Dimensional Single-Cell Mass Cytometry
Published on: December 1, 2023
Inflammatory mediators and skeletal muscle injury: a DNA microarray analysis
Mukesh Summan1, Michael McKinstry, Gordon L Warren
1Toxicology & Molecular Biology Branch, National Institute for Occupational Safety and Health, Morgantown, WV 26505-2888, USA.
Abstract:
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.
Insights
Traumatic muscle injury triggers inflammation and cell proliferation, with downregulated metabolic pathways. Monocyte chemoattractant protein-1 (MCP-1) is key in early muscle repair and recovery.
Area of Science:
- Muscle regeneration and repair
- Molecular biology of injury response
Background:
- Skeletal muscle injury involves degeneration, inflammation, regeneration, and fibrosis.
- The precise role of early inflammatory responses in muscle healing remains unclear.
Purpose of the Study:
- To investigate gene expression changes during the early stages of traumatic skeletal muscle injury.
- To identify candidate genes involved in the initial cellular events of muscle repair.
Main Methods:
- Oligonucleotide microarray analysis of mouse tibialis anterior (TA) muscle 24 hours post-injury.
- Differential gene expression analysis (fold change ≥ 1.7, p < 0.05) for 732 genes.
- Validation of selected gene expression patterns using real-time reverse transcription-polymerase chain reaction (RT-PCR), RNase protection assay (RPA), and immunohistochemistry.
Main Results:
- 2.8% of analyzed genes were upregulated, primarily related to inflammation, oxidative stress, and cell proliferation.
- 3.2% of analyzed genes were downregulated, associated with metabolic and cell signaling pathways.
- Chemokines, including monocyte chemoattractant protein-1 (MCP-1), were highly expressed, suggesting a role in monocyte/macrophage recruitment.
Conclusions:
- Early traumatic muscle injury significantly alters gene expression profiles.
- Inflammatory and cell proliferation pathways are activated, while metabolic pathways are suppressed.
- MCP-1 expression indicates a crucial role for inflammatory cell infiltration in muscle injury and recovery.
