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Updated: Jun 3, 2026

CRISPR/Cas9 Technology in Restoring Dystrophin Expression in iPSC-Derived Muscle Progenitors
Published on: September 14, 2019
Serum calcium-decreasing factor, caldecrin, ameliorates muscular dystrophy in dy/dy mice
Mineko Tomomura1, Takeru Fujii, Hiroshi Sakagami
1Division of Biochemistry, Department of Oral Biology and Tissue Engineering, Meikai University School of Dentistry, 1-1 Keyakidai, Sakado, Saitama 350-0283 Japan. atomomu@dent.meikai.ac.jp
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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