Age-related dystrophin-glycoprotein complex structure and function in the rat extensor digitorum longus and soleus muscle.
نویسندگان
چکیده
This study tested the hypothesis that age-related changes in the dystrophin-glycoprotein complex (DGC) may precede age-associated alterations in muscle morphology and function. Compared to those in adult (6 month) rats, extensor digitorum longus (EDL) and soleus muscle mass was decreased in old (30 month) and very old (36 month) Fischer 344/NNiaHSD x Brown Norway/BiNia rats. The amount of dystrophin, beta-dystroglycan, and alpha-sarcoglycan increased with aging in the EDL and decreased with aging in the soleus. alpha-Dystroglycan levels were increased with aging in both muscles and displayed evidence of altered glycosylation. Immunostaining for the presence of antibody infiltration and dystrophin following increased muscle stretch suggested that the aging in the soleus was characterized by diminished membrane integrity. Together, these data suggest that aging is associated with alterations in EDL and soleus DGC protein content and localization. These results may implicate the DGC as playing a role in age-associated skeletal muscle remodeling.
منابع مشابه
Cytoskeletal protein contents before and after hindlimb suspension in a fast and slow rat skeletal muscle.
Transversal cytoskeletal organization of muscle fibers is well described, although very few data are available concerning protein content. Measurements of desmin, alpha-actinin, and actin contents in soleus and extensor digitorum longus (EDL) rat skeletal muscles, taken with the results previously reported for several dystrophin-glycoprotein complex (DGC) components, indicate that the contents ...
متن کاملThe Fate of Dystrophin and Some Signs of Apoptosis in the Skeletal Muscle Work-Overloaded in Extension
Rat muscles, soleus and extensor digitorum longus (EDL), were eccentrically electrostimulated at low frequency for 4-24h. The cryostat-sections of these muscles were examined by immunohistochemistry. Numerous muscle fibres were damaged and necrotic. Simultaneously, several preserved fibres were not stained, or stained only discontinuously, with the anti-dystrophin and anti-p-dystroglycan antibo...
متن کاملComparative proteomic profiling of soleus, extensor digitorum longus, flexor digitorum brevis and interosseus muscles from the mdx mouse model of Duchenne muscular dystrophy
Duchenne muscular dystrophy is due to genetic abnormalities in the dystrophin gene and represents one of the most frequent genetic childhood diseases. In the X-linked muscular dystrophy (mdx) mouse model of dystrophinopathy, different subtypes of skeletal muscles are affected to a varying degree albeit the same single base substitution within exon 23 of the dystrophin gene. Thus, to determine p...
متن کاملLife-long calorie restriction in Fischer 344 rats attenuates age-related loss in skeletal muscle-specific force and reduces extracellular space.
The decline in muscle function is associated with an age-related decrease in muscle mass and an age-related decline in strength. However, decreased strength is not solely due to decreased muscle mass. The age-related decline in muscle-specific force (force/muscle cross-sectional area), a measure of intrinsic muscle function, also contributes to age-related strength decline, and the mechanisms b...
متن کاملAlpha 7 integrin preserves the function of the extensor digitorum longus muscle in dystrophin-null mice.
The dystrophin-associated glycoprotein complex (DGC) and the α7β1-integrin complex are two independent protein complexes that link the extracellular matrix with the cytoskeleton in muscle cells. These associations stabilize the sarcolemma during force transmission. Loss of either one of these complexes leads to muscular dystrophy. Dystrophin is a major component of the DGC. Its absence results ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- The journals of gerontology. Series A, Biological sciences and medical sciences
دوره 61 11 شماره
صفحات -
تاریخ انتشار 2006