Creatine kinase and prostaglandin E2 release from isolated Duchenne muscle.
We studied the release of creatine kinase (CK) activity and prostaglandin E2 (PGE2) from isolated strips of biceps muscle from patients with Duchenne muscular dystrophy and nondystrophic control patients. CK release was significantly higher from the dystrophic samples than controls during the initial period of incubation, but this difference reduced with time of incubation. Immediate immersal of muscle strips into calcium-free bathing medium reduced the initial difference between the efflux from dystrophic and nondystrophic samples, whereas treatment with the calcium ionophore maintained the difference between the groups throughout the period of incubation (150 minutes). These results support the hypothesis that the lack of dystrophin in Duchenne muscle leads to damage to the tissue via a failure of calcium homeostasis. PGE2 release from the muscle strips followed a similar pattern to CK activity, supporting the possibility that, at least partly, the calcium-mediated damage involves activation of phospholipid hydrolysis.
Jackson
M J
MJ
Department of Medicine, University of Liverpool, UK.
Brooke
M H
MH
Kaiser
K
K
Edwards
R H
RH
D000293:Adolescent; D000328:Adult; D002648:Child; D002675:Child, Preschool; D003402:Creatine Kinase / Q000378:metabolism*; D015232:Dinoprostone / Q000378:metabolism*; D006801:Humans; D066298:In Vitro Techniques; D007975:Leukotriene B4 / Q000378:metabolism; D009132:Muscles / Q000378:metabolism*; D009136:Muscular Dystrophies / Q000378:metabolism*
D007975:Leukotriene B4; D003402:Creatine Kinase; D015232:Dinoprostone