[No authors listed]
BACKGROUND:Calcium signaling is important in muscular cells and abnormal Ca(2+) handling results in muscle damage. Caldecrin is a serum calcium-decreasing factor purified from pancreas. It is a chymotrypsin-type secretory protease, whereas the serum calcium-decreasing activity does not depend on its protease activity. Here, we evaluated the effect of caldecrin on dystrophia muscularis (dy/dy) mice. MATERIALS AND METHODS:Caldecrin gene in hemagglutinating virus of Japan envelop vector (10 μg/head) was single injected in the femoral muscle or daily intraperitoneal administration of caldecrin (100 μg/kg body weight) was given for 4 days in dy/dy mice. Progression of muscular dystrophy was assessed by blood urea nitrogen and Evans blue dye penetration assay. RESULTS:Ectopic expression of the caldecrin gene in the muscle of dy/dy mice reduced the level of blood urea nitrogen and improved the dystrophic progression similarly to that of caldecrin-injected mice. CONCLUSION:Caldecrin treatment is effective for preventing muscular dystrophy.
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