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Cell death and oxidative damage in inflammatory myopathies
1Division of Neuropathology, Johannes Gutenberg-University, Mainz, Germany.
Clinical Immunology and Immunopathology
|July 1, 1998
Summary
Muscle fibers in myositis do not undergo apoptosis but show increased nitric oxide synthase (NOS). This enhanced NOS may cause muscle damage, while apoptosis regulates inflammatory cells in autoimmune myopathies.
Area of Science:
- Immunology
- Cell Biology
- Neurology
Background:
- Muscle fiber apoptosis is observed in denervating disorders and muscular dystrophies.
- The role of apoptosis in autoimmune inflammatory myopathies is not fully understood.
Purpose of the Study:
- To investigate muscle fiber apoptosis in autoimmune inflammatory myopathies.
- To examine the expression of nitric oxide synthase (NOS) in muscle fibers of myositis patients.
Main Methods:
- Studied 21 patients with autoimmune inflammatory myopathies.
- Assessed muscle fiber apoptosis using DNA fragmentation and apoptosis-related protein expression.
- Evaluated inducible and neuronal nitric oxide synthase (NOS) expression in muscle fibers.
Main Results:
- No evidence of muscle fiber apoptosis was found in myositis patients.
- Significant up-regulation of inducible and neuronal NOS was observed in muscle fibers.
- Inducible NOS was localized to the sarcolemma; neuronal NOS was found in sarcoplasm of damaged/atrophic fibers.
- Inflammatory cells showed DNA fragmentation and apoptosis-related protein expression.
Conclusions:
- Muscle fiber necrosis, potentially mediated by nitric oxide production from enhanced NOS, is the primary cell death mechanism in myositis.
- Apoptosis plays a role in regulating the inflammatory cellular response in myositis.
- No distinct disease-specific patterns were observed across different myositis subtypes.
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