Inclusion body myositis: abnormal protein accumulation does not trigger apoptosis.
To examine whether apoptosis may contribute to muscle fiber loss in inclusion body myositis, we used the terminal deoxynucleotidyl transferase-mediated X-dUTP nick-end labeling (TUNEL) assay to compare the occurrence of DNA fragmentation in muscle samples from patients with inclusion body myositis and polymyositis. TUNEL-positive nuclei in nonnecrotic muscle fibers were rare even in the vicinity of amyloid-like material; significantly more frequent in polymyositis than inclusion body myositis; and several times less frequent than necrotic muscle fibers or mononuclear cell myocytotoxicity in both patient groups. Apoptosis is unlikely to play a significant role in the pathogenesis of inclusion body myositis.
Hutchinson
D O
DO
Department of Neurology, Auckland Hospital, New Zealand.
D000368:Aged; D000686:Amyloidosis / Q000473:pathology; D017209:Apoptosis / Q000502:physiology*; D053938:DNA Fragmentation; D005260:Female; D006801:Humans; D020287:In Situ Nick-End Labeling; D002479:Inclusion Bodies / Q000737:chemistry / Q000473:pathology*; D017493:Leukocyte Common Antigens / Q000032:analysis; D008297:Male; D008875:Middle Aged; D018485:Muscle Fibers, Skeletal / Q000737:chemistry / Q000473:pathology; D009220:Myositis / Q000473:pathology*; D009336:Necrosis
D017493:Leukocyte Common Antigens