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Induction of Acute Skeletal Muscle Regeneration by Cardiotoxin Injection
Published on: January 1, 2017
Skeletal Muscle Cell Behavior After Physical Agent Treatments
Michela Battistelli1, Sara Salucci, Michele Guescini
1DiSTeVA, Campus Scientifico "Enrico Mattei", via Cà le Suore no 2, 61029 Urbino, PU, Italy. michela.battistelli@uniurb.it.
Skeletal muscle cells undergo apoptosis from physical triggers like UVB, heat, and low pH, involving caspase pathways. Hypothermia, however, enhances autophagy, potentially preventing muscle injury and inflammation.
Area of Science:
- Cell Biology
- Muscle Physiology
Background:
- Apoptosis is crucial for skeletal muscle development and homeostasis.
- Muscle cell death is implicated in myopathies, sarcopenia, denervation, disuse, and strenuous exercise.
Purpose of the Study:
- To investigate skeletal muscle cell death induced by various physical agents in vitro.
- To analyze the morpho-functional and molecular responses of C2C12 myoblasts and myotubes to UVB, hyperthermia, low pH, and hypothermia.
Main Methods:
- C2C12 myoblasts and myotubes were exposed to UVB, hyperthermia (43°C), low pH, and hypothermia (0-6°C).
- Morphological, in situ DNA fragmentation, and molecular analyses (caspase pathway, autophagy) were performed after recovery periods.
- Cellular responses were assessed using morpho-functional and molecular approaches.
Main Results:
- UVB, hyperthermia, and low pH induced apoptosis and DNA fragmentation, with caspase involvement.
- Low pH also caused necrosis with swollen nuclei; apoptotic and necrotic nuclei were observed in the same myotube.
- Hypothermia induced minimal chromatin changes and increased autophagy, without DNA fragmentation or caspase activation.
Conclusions:
- Skeletal muscle cells are sensitive to physical agents, with UVB, hyperthermia, and acidosis inducing apoptotic cell death.
- Hypothermia promotes an autophagic response, suggesting a role in delaying muscle inflammation and injury.
- Understanding these responses provides insights into muscle cell death mechanisms and potential therapeutic strategies.
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