Abstract
In Duchenne muscular dystrophy, muscle cells, which lack the protein dystrophin, have been reported to have elevated resting intracellular calcium levels. It has also been noted that, compared to normal muscle, intracellular [Ca 2+] in dystrophic muscle returns more slowly to its resting level following contractile stimulation. Consistent with this, it has been suggested that dystrophin is directly involved in the regulation of Ca 2+ influx. A secondary alteration in the sarcoplasmic reticulum Ca 2+ pump, however, could also contribute to, or be responsible for, the abnormal Ca 2+ handling seen. To determine whether the Ca 2+ pump is functionally altered in dystrophic muscle, we examined Ca 2+ uptake by vesicles derived from skeletal muscle sarcoplasmic reticulum of normal and dystrophic (mdx) mice. The Hill coefficient and the Ca 2+ sensitivity of the Ca 2+-ATPase were the same in both cases. The maximum velocity of Ca 2+ uptake, however, normalized to the ATPase content of the vesicles, was less for mdx muscle.
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Schedule a callMore From: Biochimica et Biophysica Acta (BBA) - General Subjects
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