Expression of Bcl-2 in inclusion body myositis

Acta Neurol Scand. 2002 May;105(5):403-7. doi: 10.1034/j.1600-0404.2002.01198.x.

Abstract

Objectives: On the background of the possible role of the anti-apoptotic protein Bcl-2 to inhibit apoptosis induced by the Fas/Fas ligand system in inflammatory myopathies we investigated the expression of Bcl-2 in inclusion body myositis (IBM).

Material and methods: We examined muscle tissue from seven IBM patients and controls by immunocytochemistry using antibodies against Bcl-2, Fas (a member of the tumor necrosis factor receptor family) and the regeneration marker, neural cell adhesion molecule (N-CAM). We also investigated the occurrence of DNA fragmentation by the terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL)-method.

Results: Both Bcl-2 and Fas were up-regulated in muscle fibers in IBM and disease controls. Bcl-2 was expressed by regenerating muscle fibers while Fas was expressed by non-regenerating muscle fibers associated with inflammatory cell infiltrates. Bcl-2 and Fas were also expressed by inflammatory cells. There were scattered TUNEL positive nuclei and most of these appeared to be inflammatory cells.

Conclusion: The low occurrence of apoptotic myonuclei is not related to Bcl-2 expression, which is confined to regenerating muscle cells in IBM and other myopathies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing*
  • Antibodies / analysis
  • Apoptosis / genetics
  • Apoptosis / immunology
  • Biopsy
  • Carrier Proteins / genetics
  • DNA Fragmentation / genetics
  • DNA Fragmentation / immunology
  • Fas-Associated Death Domain Protein
  • Gene Expression / genetics
  • Genes, bcl-2 / genetics*
  • Genes, bcl-2 / immunology
  • Humans
  • Immunohistochemistry
  • In Situ Nick-End Labeling
  • Muscle Fibers, Skeletal / pathology
  • Muscle, Skeletal / pathology
  • Myositis, Inclusion Body / diagnosis
  • Myositis, Inclusion Body / genetics*
  • Neural Cell Adhesion Molecules / analysis
  • Neural Cell Adhesion Molecules / genetics
  • Neural Cell Adhesion Molecules / immunology

Substances

  • Adaptor Proteins, Signal Transducing
  • Antibodies
  • Carrier Proteins
  • FADD protein, human
  • Fas-Associated Death Domain Protein
  • Neural Cell Adhesion Molecules