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Expression of Bcl-2 in inclusion body myositis
Ing-Marie Fyhr1, C Lindberg, A Oldfors
1Department of Pathology, Sahlgrenska University Hospital, Göteborg University, S-413 45 Göteborg, Sweden. ingmarie.fyhr@path.gu.se
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.