{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,4]],"date-time":"2026-06-04T05:06:42Z","timestamp":1780549602477,"version":"3.54.1"},"reference-count":52,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[2010,12]]},"abstract":"<jats:p> The glycosylation of dystroglycan is required for its function as a high-affinity laminin receptor, and loss of dystroglycan glycosylation results in congenital muscular dystrophy. The purpose of this study was to investigate the functional defects in slow- and fast-twitch muscles of glycosylation-deficient Large<jats:sup>myd<\/jats:sup> mice. While a partial alteration in glycosylation of dystroglycan in heterozygous Large<jats:sup>myd\/+<\/jats:sup> mice was not sufficient to alter muscle function, homozygous Large<jats:sup>myd\/myd<\/jats:sup> mice demonstrated a marked reduction in specific force in both soleus and extensor digitorum longus (EDL) muscles. Although EDL muscles from Large<jats:sup>myd\/myd<\/jats:sup> mice were highly susceptible to lengthening contraction-induced injury, Large<jats:sup>myd\/myd<\/jats:sup> soleus muscles surprisingly showed no greater force deficit compared with wild-type soleus muscles even after five lengthening contractions. Despite no increased susceptibility to injury, Large<jats:sup>myd\/myd<\/jats:sup> soleus muscles showed loss of dystroglycan glycosylation and laminin binding activity and dystrophic pathology. Interestingly, we show that soleus muscles have a markedly higher sarcolemma expression of \u03b2<jats:sub>1<\/jats:sub>-containing integrins compared with EDL and gastrocnemius muscles. Therefore, we conclude that \u03b2<jats:sub>1<\/jats:sub>-containing integrins play an important role as matrix receptors in protecting muscles containing slow-twitch fibers from contraction-induced injury in the absence of dystroglycan function, and that contraction-induced injury appears to be a separable phenotype from the dystrophic pathology of muscular dystrophy. <\/jats:p>","DOI":"10.1152\/ajpcell.00192.2010","type":"journal-article","created":{"date-parts":[[2010,9,16]],"date-time":"2010-09-16T02:39:44Z","timestamp":1284604784000},"page":"C1430-C1440","source":"Crossref","is-referenced-by-count":21,"title":["Soleus muscle in glycosylation-deficient muscular dystrophy is protected from contraction-induced injury"],"prefix":"10.1152","volume":"299","author":[{"given":"Jessica D.","family":"Gumerson","sequence":"first","affiliation":[{"name":"Department of Molecular & Integrative Physiology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhyldyz 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