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新着情報 |
ミツグミン２９と筋老化の関係 〜国際共同研究の成果より (2006. 8)
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Muscle
aging is associated with compromised Ca2+ spark signaling
and segregated intracellular Ca2+ release
(J. Cell Biol. 174, 639-645, 2006)
Noah Weisleder, Marco Brotto, Shinji Komazaki, Zui Pan,
Xiaoli Zhao,
Thomas Nosek,
Jerome Parness, Hiroshi Takeshima and Jianjie Ma
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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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