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Telomere shortening in diaphragm and tibialis anterior muscles of aged mdx mice
Author(s) -
Lund Troy C.,
Grange Robert W.,
Lowe Dawn A.
Publication year - 2007
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.20824
Subject(s) - telomere , duchenne muscular dystrophy , senescence , diaphragm (acoustics) , biology , muscular dystrophy , mdx mouse , anatomy , tibialis anterior muscle , cellular aging , skeletal muscle , endocrinology , medicine , microbiology and biotechnology , dystrophin , genetics , dna , physics , acoustics , loudspeaker
The progression of Duchenne muscular dystrophy (DMD) is, in part, due to satellite cell senescence driven by high replicative pressure as these muscle stem cells repeatedly divide and fuse to damaged muscle fibers. We hypothesize that telomere shortening in satellite cells underlies their senescence. To test this hypothesis, we evaluated the diaphragm and a leg muscle from dystrophic mice of various ages for telomere dynamics. We found 30% telomere shortening in tibialis anterior muscles from 600‐day‐old mdx mice relative to age‐matched wildtype mice. We also found a more severe shortening of telomere length in diaphragm muscles of old mdx mice. In those muscles, telomeres were shortened by ∼15% and 40% in 100‐ and 600‐day‐old mdx mice, respectively. These findings indicate that satellite cells undergo telomere erosion, which may contribute to the inability of these cells to perpetually repair DMD muscle. Muscle Nerve, 2007