Journal
JOURNAL OF CELL BIOLOGY
Volume 174, Issue 5, Pages 639-645Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200604166
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Funding
- NCI NIH HHS [R01 CA095739, R01-CA95739] Funding Source: Medline
- NHLBI NIH HHS [R01-HL69000, R01 HL069000] Funding Source: Medline
- NIAMS NIH HHS [R01-AR45593, R01 AR045593] Funding Source: Medline
- NIA NIH HHS [R01 AG028614, R01-AG15556, R01-AG28614, R01 AG015556] Funding Source: Medline
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Reduced homeostatic capacity for intracellular Ca2+ ([Ca2+](i)) movement may underlie the progression of sarcopenia and contractile dysfunction during muscle aging. We report two alterations to Ca2+ homeostasis in skeletal muscle that are associated with aging. Ca2+ sparks, which are the elemental units of Ca2+ release from sarcoplasmic reticulum, are silent under resting conditions in young muscle, yet activate in a dynamic manner upon deformation of membrane structures. The dynamic nature of Ca2+ sparks appears to be lost in aged skeletal muscle. Using repetitive voltage stimulation on isolated muscle preparations, we identify a segregated [ Ca2+] i reserve that uncouples from the normal excitation - contraction process in aged skeletal muscle. Similar phenotypes are observed in adolescent muscle null for a synaptophysin-family protein named mitsugumin-29 (MG29) that is involved in maintenance of muscle membrane ultrastructure and Ca2+ signaling. This finding, coupled with decreased expression of MG29 in aged skeletal muscle, suggests that MG29 expression is important in maintaining skeletal muscle Ca2+ homeostasis during aging.
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