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Differences in contraction‐induced injury in fast and slow muscles in glycosylation‐deficient muscular dystrophy
Author(s) -
Gumerson Jessica Delores,
Kabaeva Zhyldyz T,
Davis Carol S,
John Jeswin B,
Faulkner John A,
Michele Daniel E
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1051.34
Subject(s) - soleus muscle , itga7 , downregulation and upregulation , dystrophin , muscular dystrophy , medicine , myocyte , endocrinology , chemistry , myosin , muscle contraction , microbiology and biotechnology , skeletal muscle , biology , biochemistry , gene
Susceptibility of muscle to contraction‐induced (CI) injury is considered a hallmark of dystrophin glycoprotein complex associated muscular dystrophies. We investigated how loss of dystroglycan matrix receptor function in glycosylation‐deficient mice impacted muscle contractile function. Soleus and extensor digitorum longus (EDL) muscles from Large myd/myd mice both demonstrated reduced specific force but surprisingly, only the EDL muscle was more susceptible to lengthening CI injury. Large myd/myd soleus muscle showed no increase in force deficit when compared to WT soleus muscle but still showed histological features of dystrophic pathology similar to fast muscle. This suggests that increased CI injury is not the primary mechanism for the observed muscle degeneration. One possible explanation for the lack of increased CI injury is that soleus muscle exhibits higher expression of an alternative matrix receptor, α7β1 integrin. Interestingly, Large myd/myd dystrophic fast muscles show fiber type conversion indicated by increased slow‐twitch and hybrid fibers, and a concomitant increase in β1 integrin expression compared to WT muscle. Therefore, slow fiber type conversion in dystrophic muscle and a corresponding upregulation of β1 integrin expression might be an important compensatory mechanism in dystrophic muscle that could be targeted for prevention of muscle injury.