期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 288, 期 4, 页码 2103-2109出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M112.425975
关键词
-
资金
- National Institutes of Health [AG28614, AG28856, HL69000, AR054793]
Functional coupling between inositol (1,4,5)-trisphosphate receptor (IP3R) and ryanodine receptor (RyR) represents a critical component of intracellular Ca2+ signaling in many excitable cells; however, the role of this mechanism in skeletal muscle remains elusive. In skeletal muscle, RyR-mediated Ca2+ sparks are suppressed in resting conditions, whereas application of transient osmotic stress can trigger activation of Ca2+ sparks that are restricted to the periphery of the fiber. Here we show that onset of these spatially confined Ca2+ sparks involves interaction between activation of IP3R and RyR near the sarcolemmal membrane. Pharmacological prevention of IP3 production or inhibition of IP3R channel activity abolishes stress-induced Ca2+ sparks in skeletal muscle. Although genetic ablation of the type 2 IP3R does not appear to affect Ca2+ sparks in skeletal muscle, specific silencing of the type 1 IP3R leads to ablation of stress-induced Ca2+ sparks. Our data indicate that membrane-delimited signaling involving cross-talk between IP(3)R1 and RyR1 contributes to Ca2+ spark activation in skeletal muscle.
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