Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10873625 | FEBS Letters | 2005 | 6 Pages |
Abstract
Muscle fibers attach to laminin in the basal lamina using two mechanisms, i.e., dystrophin with its associated proteins and α7β1 integrin. In humans, gene-mutation defects in one member of these complexes result in muscular dystrophies. This study revealed changes after l-arginine treatment of utrophin-associated proteins and the α7B integrin subunit in mdx mouse, a dystrophin-deficient animal model. In the two studied muscles (cardiac muscle and diaphragm), the α7B integrin subunit was increased in 5-week-old treated mice. Interestingly, the diaphragm histopathological appearance was significantly improved by l-arginine administration. These results highlight a possible way to compensate for dystrophin deficiency via α7β1 integrin.
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Authors
Delphine Chazalette, Karim Hnia, François Rivier, Gérald Hugon, Dominique Mornet,