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In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells
Published on: June 12, 2017
Paraplegia increases skeletal muscle autophagy
Christopher S Fry1, Micah J Drummond, Heidi L Lujan
1Division of Rehabilitation Sciences, University of Texas Medical Branch, Galveston, Texas 77555-1144, USA.
Muscle & Nerve
|October 12, 2012
Summary
Paraplegia causes severe skeletal muscle atrophy by increasing protein breakdown. This study found autophagy increases in paraplegic rats, independent of SIRT1 signaling, suggesting a negative impact on muscle protein balance.
Area of Science:
- Physiology
- Molecular Biology
- Cellular Biology
Background:
- Paraplegia leads to significant skeletal muscle atrophy.
- This atrophy is linked to increased protein breakdown.
- The SIRT1-p53 pathway's role in regulating autophagy and protein breakdown is a recent discovery.
Purpose of the Study:
- To investigate the impact of chronic paraplegia on skeletal muscle autophagy.
- To explore the role of the SIRT1-p53 pathway in paraplegia-induced muscle atrophy.
Main Methods:
- Soleus muscles were collected from paraplegic and control rats.
- Immunoblotting was used to measure intracellular proteins.
- Quantitative real-time PCR measured skeletal muscle microRNA expression.
Main Results:
- SIRT1 protein expression was significantly lower in paraplegic rats.
- p53 acetylation (LYS379) was increased in paraplegic rats.
- Markers of autophagy induction (Atg7 and Beclin-1) were elevated in paraplegic rats.
Conclusions:
- Skeletal muscle autophagy increases in chronic paraplegia, independent of SIRT1 signaling.
- Chronic paraplegia may lead to increased autophagic cell death.
- This process negatively impacts skeletal muscle protein balance.
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