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Apoptosis in atrophic skeletal muscle induced by brachial plexus injury in rats
1Department of Pathophysiology, Shanghai Medical University, 130 Yixueyuan Road, Shanghai 200032, People's Republic of China.
Background:
Skeletal muscle atrophy induced by denervation is associated with apoptosis. This study was undertaken to determine the role of apoptosis and the expression of apoptosis-associated genes in rat skeletal muscle made atrophic by brachial plexus injury, and to study the apoptotic signal transduction pathway.
Methods:
An animal model of skeletal muscle atrophy was established in rats by severing the brachial plexus of one forelimb. Apoptosis of muscle cells was investigated with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate end labeling, flow cytometry, deoxyribonucleic acid (DNA) electrophoresis, and electron microscopy. The apoptosis-associated genes Fas, FADD, Caspase 8, c-myc, p53, and Bcl-2 were detected by immunohistochemistry and Northern blot.
Results:
By terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate end labeling and flow cytometry we found that the percentage of apoptotic muscle cells was higher in atrophic than in healthy skeletal muscle (p < 0.05). DNA laddering could be seen in gel electrophoresis of DNA from atrophic muscle. By electron microscopy, we observed morphologic change of early apoptosis, such as aggregation of chromosomes, expansion of nucleic cistern, and contraction of the nucleus. Using immunohistochemistry, we determined that in atrophic muscle Fas, FADD, and Caspase-8 genes were highly expressed, whereas Bcl-2 was poorly expressed (p < 0.01). However, we did not detect a change in the expression of p53 or c-myc genes. Northern blots indicated that Fas messenger ribonucleic acid was higher and Bcl-2 messenger ribonucleic acid was lower in atrophic than in healthy muscle (p < 0.01).
Conclusion:
There are many more apoptotic cells in muscle atrophied as a result of brachial plexus injury than in healthy muscle, and apoptosis plays an important role in the pathogenesis of atrophy. The apoptotic signal may be transmitted from Fas to FADD to Caspase-8, with a decrease in Bcl-2 expression aggravating the process.
Insights
Denervation-induced skeletal muscle atrophy involves increased apoptosis. Brachial plexus injury in rats showed elevated apoptotic cells and specific gene expression changes, highlighting apoptosis
Area of Science:
- Cell Biology
- Molecular Biology
- Physiology
Background:
- Skeletal muscle atrophy following denervation is linked to programmed cell death (apoptosis).
- Investigating apoptosis and related gene expression in denervated muscle is crucial for understanding atrophy pathogenesis.
Purpose of the Study:
- To determine the role of apoptosis in rat skeletal muscle atrophy induced by brachial plexus injury.
- To analyze the expression of apoptosis-associated genes and the apoptotic signal transduction pathway.
Main Methods:
- Established a rat model of skeletal muscle atrophy via brachial plexus severing.
- Assessed muscle cell apoptosis using TUNL assay, flow cytometry, DNA electrophoresis, and electron microscopy.
- Quantified apoptosis-associated gene expression (Fas, FADD, Caspase-8, c-myc, p53, Bcl-2) via immunohistochemistry and Northern blot.
Main Results:
- Apoptotic muscle cells were significantly increased in atrophic compared to healthy muscle (p < 0.05).
- Morphological evidence of early apoptosis and DNA laddering confirmed cell death.
- Upregulation of Fas, FADD, and Caspase-8, and downregulation of Bcl-2 were observed in atrophic muscle (p < 0.01).
- No significant changes in p53 or c-myc gene expression were detected.
Conclusions:
- Apoptosis plays a significant role in the pathogenesis of skeletal muscle atrophy after brachial plexus injury.
- The apoptotic pathway involves Fas, FADD, and Caspase-8 signaling, exacerbated by reduced Bcl-2 expression.
