肌动蛋白细胞骨架差异性调节NG115 - 401L细胞的雷诺丁受体和肌醇1,4,5 - 三磷酸受体诱导的钙信号通路。
The actin cytoskeleton differentially regulates NG115-401L cell ryanodine receptor and inositol 1,4,5-trisphosphate receptor induced calcium signaling pathways.
作者信息
Bose Diptiman D, Thomas David W
机构信息
Department of Molecular Biosciences School of Veterinary Medicine, University of California, Davis, CA 95616, USA.
出版信息
Biochem Biophys Res Commun. 2009 Feb 6;379(2):594-9. doi: 10.1016/j.bbrc.2008.12.138. Epub 2009 Jan 4.
Regulation of bi-directional communication between intracellular Ca(2+) pools and surface Ca(2+) channels remains incompletely characterized. We report Ca(2+) release mediated by inositol 1,4,5-trisphosphate receptor (IP(3)R) and ryanodine receptor (RyR) pathways is diminished under actin cytoskeleton disruption in NG115-401L (401L) neuronal cells, yet despite truncated Ca(2+) release, Ca(2+) influx was not significantly altered in these experiments. However, disruption of cortical actin networks completely abolished IP(3)R induced Ca(2+) release, whereas RyR-mediated Ca(2+) release was preserved, albeit attenuated. Moreover, cortical actin disruption completely abolished IP(3)R and RyR linked Ca(2+) influx even though Ca(2+) pool sensitivities were different. These findings suggest discrete Ca(2+) store/Ca(2+) channel coupling mechanisms in the IP(3)R and RyR pathways as revealed by the differential sensitivity to actin perturbation.
细胞内钙库与表面钙通道之间双向通讯的调节机制尚未完全明确。我们报道，在NG115 - 401L（401L）神经元细胞中，肌动蛋白细胞骨架破坏时，由肌醇1,4,5 - 三磷酸受体（IP₃R）和兰尼碱受体（RyR）途径介导的钙释放减少，然而，尽管钙释放被截断，但在这些实验中钙内流并未显著改变。然而，皮质肌动蛋白网络的破坏完全消除了IP₃R诱导的钙释放，而RyR介导的钙释放得以保留，尽管有所减弱。此外，尽管钙库敏感性不同，但皮质肌动蛋白破坏完全消除了IP₃R和RyR相关的钙内流。这些发现表明，IP₃R和RyR途径中存在离散的钙库/钙通道偶联机制，这通过对肌动蛋白扰动的不同敏感性得以揭示。
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