Open AccessCompromised store‐operated Ca 2+ entry in aged skeletal muscle
Author(s) -
Zhao Xiaoli,
Weisleder Noah,
Thornton Angela,
Oppong Yaa,
Campbell Rachel,
Ma Jianjie,
Brotto Marco
Publication year - 2008
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/j.1474-9726.2008.00408.x
Subject(s) - skeletal muscle , biology , endocrinology , medicine , homeostasis , extracellular , myocyte , intracellular , sarcopenia , microbiology and biotechnology
Summary In aged skeletal muscle, changes to the composition and function of the contractile machinery cannot fully explain the observed decrease in the specific force produced by the contractile machinery that characterizes muscle weakness during aging. Since modification in extracellular Ca 2+ entry in aged nonexcitable and excitable cells has been recently identified, we evaluated the functional status of store‐operated Ca 2+ entry (SOCE) in aged mouse skeletal muscle. Using Mn 2+ quenching of Fura‐2 fluorescence and confocal‐microscopic imaging of Ca 2+ movement from the transverse tubules, we determined that SOCE was severely compromised in muscle fibers isolated from aged mice (26–27 months) as compared with those from young (2–5 months) mice. While reduced SOCE in aged skeletal muscle does not appear to result from altered expression levels of STIM1 or reduced expression of mRNA for Orai, this reduction in SOCE is mirrored in fibers isolated from young mice null for mitsugumin‐29, a synaptophysin‐related protein that displays decreased expression in aged skeletal muscle. Our data suggest that decreased mitsugumin‐29 expression and reduced SOCE may contribute to the diminished intracellular Ca 2+ homeostatic capacity generally associated with muscle aging.