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Muscle sparing in muscle RING finger 1 null mice: response to synthetic glucocorticoids
Author(s) -
Baehr Leslie M.,
Furlow J. David,
Bodine Sue C.
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.212845
Subject(s) - muscle atrophy , denervation , medicine , atrophy , endocrinology , gastrocnemius muscle , glucocorticoid , dexamethasone , protein degradation , chemistry , cycloheximide , skeletal muscle , protein biosynthesis , biochemistry
Non‐Technical Summary Skeletal muscle has the capacity to modify its size in response to external cues such as mechanical load, neural activity, hormones, stress and nutritional status. Pathological muscle loss or ‘atrophy’ occurs as the result of a number of disparate conditions including ageing, immobilization, diabetes, cancer, sepsis and as a serious side effect of corticosteroid hormone treatment. Synthetic glucocorticoids are often used to treat inflammation; however, high doses and chronic use of these hormones can lead to the loss of skeletal muscle mass and weakness. We show that in mice with a deletion of the MuRF1 protein, but not the MAFbx protein, the loss of muscle mass is attenuated relative to normal mice following 14 days of glucocorticoid treatment. Knowledge of how the MuRF1 protein functions in skeletal muscle to regulate skeletal muscle mass could lead to the development of therapeutics to prevent muscle atrophy under various conditions including glucocorticoid treatment.