Compromised store-operated Ca2+ entry in aged skeletal muscle.
Compromised store-operated Ca2+ entry in aged skeletal muscle.
复制标题
衰老骨骼肌中钙池操纵的 Ca2+ 进入受损。
DOI:
10.1111/j.1474-9726.2008.00408.x
复制
发表时间:
2008-08
期刊:
影响因子:
7.8
通讯作者:
Brotto, Marco
中科院分区:
文献类型:
--
作者:
Zhao, Xiaoli;Weisleder, Noah;Thornton, Angela;Oppong, Yaa;Campbell, Rachel;Ma, Jianjie;Brotto, Marco
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 Ca2+ entry in aged nonexcitable and excitable cells has been recently identified, we evaluated the functional status of store-operated Ca2+ entry (SOCE) in aged mouse skeletal muscle. Using Mn2+ quenching of Fura-2 fluorescence and confocal-microscopic imaging of Ca2+ 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 Ca2+ homeostatic capacity generally associated with muscle aging.
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影响因子:
2.1
作者:
DANGAIN, J;NEERING, IR
通讯作者:
NEERING, IR
影响因子:
56.9
作者:
FONG, P;TURNER, PR;STEINHARDT, RA
通讯作者:
STEINHARDT, RA
影响因子:
3.4
作者:
Collet, C;Ma, JJ
通讯作者:
Ma, JJ
影响因子:
2.4
作者:
González, E;Messi, ML;Delbono, O
通讯作者:
Delbono, O
DOI:
10.1016/j.bbrc.2003.09.146
发表时间:
2003-10-31
影响因子:
3.1
作者:
Kurebayashi, N;Takeshima, H;Ogawa, Y
通讯作者:
Ogawa, Y