Brain, Vol 120, Issue 6 929-938, Copyright © 1997 by Oxford University Press
L Behrens, A Bender, MA Johnson and R Hohlfeld
Expression of the Fas 'death receptor', Fas (CD95/APO-1) renders cells
susceptible to programmed cell death ('apoptosis'), whereas Bcl-2 protects
cells from apoptosis. Using fluorescence immunohistochemistry, we analysed
Fas and Bcl-2 expression in muscle from five patients with polymyositis
(PM), four patients with inclusion body myositis (IBM), three patients with
dermatomyositis (DM), three patients with Duchenne muscular dystrophy (DMD)
and three nonmyopathic controls. Fas (CD95) and Bcl-2 were not detected in
control muscle, but expressed in muscle fibres and inflammatory cells in
PM, IBM, DM and DMD. The proportion of Fas+ muscle fibres ranged from <
1 to 50%, and was higher in PM and IBM than in DM and DMD. On average, the
Fas+ muscle fibres were smaller (median diameter, 10 microns; range, 7-32
microns) than the Fas- fibres (median, 36 microns; range, 10-60 microns).
Less than 10% of the Fas+ muscle fibres co-expressed the regeneration
marker CD56 (neural cell adhesion molecule N-CAM). In PM and IBM, the
proportion of Fas+ muscle fibres was higher among fibres invaded or
contacted by T cells than among fibres not contacted by T cells (P <
0.01). The proportion of Fas+ fibres co-expressing Bcl-2 was 76 +/- 16% in
PM, 100% in IBM and 63 +/- 23% in DM. Fas and Bcl-2 expression was also
noted in inflammatory cells in PM, IBM, DM and DMD. Using the terminal
deoxytransferase-catalysed DNA nick end labelling technique for detection
of nuclear DNA fragmentation, none of myonuclei, and < 0.1% of
inflammatory cell nuclei, showed signs of apoptosis. Our results suggest
that, although Fas expression confers susceptibility to Fas- mediated
apoptosis, Fas-expressing muscle fibres and inflammatory cells are
protected by the anti-apoptotic protein Bcl-2.
ARTICLES
Cytotoxic mechanisms in inflammatory myopathies. Co-expression of Fas and protective Bcl-2 in muscle fibres and inflammatory cells
Department of Neuroimmunology, Max-Planck Institute, Martinsried, Germany.
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