NDLI: Soleus muscle in glycosylation-deficient muscular dystrophy is protected from contraction-induced injury.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gumerson, Jessica D. Kabaeva, Zhyldyz T. Davis, Carol S. Faulkner, John A. Michele, Daniel E.
Description	Country affiliation: United States Author Affiliation: Gumerson JD ( Department of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, Michigan 48109-0622, USA.)
Abstract	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(myd) mice. While a partial alteration in glycosylation of dystroglycan in heterozygous Large(myd/+) mice was not sufficient to alter muscle function, homozygous Large(myd/myd) mice demonstrated a marked reduction in specific force in both soleus and extensor digitorum longus (EDL) muscles. Although EDL muscles from Large(myd/myd) mice were highly susceptible to lengthening contraction-induced injury, Large(myd/myd) 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(myd/myd) 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 ß(1)-containing integrins compared with EDL and gastrocnemius muscles. Therefore, we conclude that ß(1)-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.
File Format	HTM / HTML
ISSN	03636143
e-ISSN	15221563
DOI	10.1152/ajpcell.00192.2010
Journal	American Journal of Physiology - Cell Physiology
Issue Number	6
Volume Number	299
Language	English
Publisher	American Physiological Society
Publisher Date	2010-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Dystroglycans Metabolism Muscle Contraction Muscle, Skeletal Injuries Physiopathology Muscular Dystrophy, Animal Animals Antigens, Cd29 Glycosylation Laminin Mice Muscle Fibers, Fast-twitch Pathology Muscle Fibers, Slow-twitch Rats, Sprague-dawley Sarcolemma Research Support, N.i.h., Extramural
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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