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Fas mediates apoptosis in steroid-induced myopathy of rats.

Abstract
Recently, apoptotic cell death has been reported in differentiated skeletal muscle, where apoptosis was generally assumed not to occur. To investigate whether apoptosis may contribute to the steroid-induced myopathy, rats treated with triamcinolone acetonide (TA) for 9 days were sacrificed for detecting apoptosis by in situ end-labelling (ISEL) and DNA electrophoresis in soleus muscles. Immunohistochemical stainings of Fas antigen and p53 protein were performed to examine whether apoptosis-related proteins were present in the myopathy. Muscle fibre necrosis and apoptotic myonuclei appeared in soleus muscles following administration of TA, while control muscles showed no evidences for apoptosis. Fas antigen was not detected in control muscles, but expressed in soleus muscles of steroid-induced myopathy. Some of the Fas antigen-expressing muscle fibres were positive for ISEL. p53 Protein was not detected in any muscle fibres. These findings indicate that TA can induce apoptosis in differentiated skeletal muscles, and Fas antigen might be partly related to apoptotic muscle death in steroid-induced myopathy.
AuthorsM C Lee, J S Lee, M J Lee, J H Lee, H I Kim
JournalNeuropathology and applied neurobiology (Neuropathol Appl Neurobiol) Vol. 27 Issue 5 Pg. 396-402 (Oct 2001) ISSN: 0305-1846 [Print] England
PMID11679091 (Publication Type: Journal Article)
Chemical References
  • Anti-Inflammatory Agents
  • Tumor Suppressor Protein p53
  • fas Receptor
  • DNA
  • Triamcinolone Acetonide
Topics
  • Animals
  • Anti-Inflammatory Agents (pharmacology)
  • Apoptosis (physiology)
  • DNA (analysis)
  • Electrophoresis
  • Female
  • Immunohistochemistry
  • In Situ Nick-End Labeling
  • Muscle, Skeletal (chemistry, pathology)
  • Muscular Diseases (chemically induced, pathology)
  • Rats
  • Rats, Sprague-Dawley
  • Triamcinolone Acetonide (pharmacology)
  • Tumor Suppressor Protein p53 (analysis)
  • fas Receptor (analysis, metabolism)

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