A role for calcium-calmodulin in regulating nitric oxide production during skeletal muscle satellite cell activation
A role for calcium-calmodulin in regulating nitric oxide production during skeletal muscle satellite cell activation
复制标题
DOI：
10.1152/ajpcell.00471.2008
复制
发表时间：
2009-04-01
影响因子：
5.5
通讯作者：
Allen, Ronald E.
中科院分区：
文献类型：
--
作者：
Tatsumi, Ryuichi;Wuollet, Adam L.;Allen, Ronald E.
Tatsumi R，Wuollet AL，Tabata K，Nishimura S，Tabata S，Mizunoya W，Ikeuchi Y，艾伦RE.钙-钙调素在骨骼肌卫星细胞活化过程中调节一氧化氮生成的作用。美国生理学杂志细胞生理学296：C922-C929，2009年。首次发表于2009年1月21日; doi：10.1152/ajpcell.00471.2008。当骨骼肌受到拉伸或损伤时，肌源性卫星细胞被激活进入细胞周期。该过程取决于通过NO合酶（NOS）产生的一氧化氮（NO）、基质金属蛋白酶活化、肝细胞生长因子（HGF）从细胞外基质的释放以及HGF向c-met受体的呈递，如通过原代培养和体内测定所证明的。我们现在增加的证据表明，钙-钙调蛋白参与了卫星细胞体外激活级联反应。用钙离子载体（A23187，离子霉素）处理2小时的培养物的条件培养基激活培养的卫星细胞，并含有活性HGF，类似于机械拉伸或NO供体处理的效果。加入钙调蛋白抑制剂（calmidazolium，W-13，W-12）或NOS抑制剂N-G-硝基-L-精氨酸甲酯盐酸盐可消除该反应，但其活性较低的对映体N-G-硝基-精氨酸甲酯盐酸盐不能消除该反应。卫星细胞也被证明表达功能性钙调素蛋白具有钙结合活性，在12小时postplating，这是在本研究中加入钙离子载体的时间和拉伸处理应用在我们以前的实验。因此，从这些实验的结果提供了一个额外的见解，钙-钙调蛋白介导的基质中的HGF的释放，这一步骤的激活途径是从NO合成的上游。
Tatsumi R, Wuollet AL, Tabata K, Nishimura S, Tabata S, Mizunoya W, Ikeuchi Y, Allen RE. A role for calcium-calmodulin in regulating nitric oxide production during skeletal muscle satellite cell activation. Am J Physiol Cell Physiol 296: C922-C929, 2009. First published January 21, 2009; doi:10.1152/ajpcell.00471.2008.-When skeletal muscle is stretched or injured, myogenic satellite cells are activated to enter the cell cycle. This process depends on nitric oxide (NO) production by NO synthase (NOS), matrix metalloproteinase activation, release of hepatocyte growth factor (HGF) from the extracellular matrix, and presentation of HGF to the c-met receptor as demonstrated by a primary culture and in vivo assays. We now add evidence that calcium-calmodulin is involved in the satellite cell activation cascade in vitro. Conditioned medium from cultures that were treated with a calcium ionophore (A23187, ionomycin) for 2 h activated cultured satellite cells and contained active HGF, similar to the effect of mechanical stretch or NO donor treatments. The response was abolished by addition of calmodulin inhibitors (calmidazolium, W-13, W-12) or a NOS inhibitor N-G-nitro-L-arginine methyl ester hydrochloride but not by its less inactive enantiomer N-G-nitro-Darginine methyl ester hydrochloride. Satellite cells were also shown to express functional calmodulin protein having a calcium-binding activity at 12 h postplating, which is the time at which the calcium ionophore was added in this study and the stretch treatment was applied in our previous experiments. Therefore, results from these experiments provide an additional insight that calcium-calmodulin mediates HGF release from the matrix and that this step in the activation pathway is upstream from NO synthesis.