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首页> 外文期刊>Journal of Cellular Physiology >Low-power laser irradiation activates Src tyrosine kinase through reactive oxygen species-mediated signaling pathway.
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Low-power laser irradiation activates Src tyrosine kinase through reactive oxygen species-mediated signaling pathway.

机译：低功率激光照射激活Src酪氨酸通过活性氧species-mediated激酶信号通路。

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摘要

Low-power laser therapy in medicine is widespread but the mechanisms are not fully understood. It has been suggested that low-power laser irradiation (LPLI) could induce photochemical reaction and activate several intracellular signaling pathways. Reactive oxygen species (ROS) are considered to be the key secondary messengers produced by LPLI. Here, we studied the signaling pathway mediated by ROS upon the stimulation of LPLI. Src tyrosine kinases are well-known targets of ROS and can be activated by oxidative events. Using a Src reporter based on fluorescence resonance energy transfer (FRET) and confocal laser scanning microscope, we visualized the dynamic Src activation in Hela cells immediately after LPLI. Moreover, Src activation by LPLI was in a dose-dependent manner. The increase of Src phosphorylation at Tyr416 was detected by Western blotting. In the presence of vitamin C, catalase alone, or the combination of catalase and superoxide dismutase (SOD), the activation of Src by LPLI is significantly abolished. In contrast, Go6983 loading, a PKC inhibitor, did not affect this response. Treatment of Hela cells with exogenous H(2)O(2) also resulted in a concentration-dependent activation of Src. These results demonstrated that it was ROS that mediated Src activation by LPLI. Cellular viability assay revealed that laser irradiation of low doses (
机译：低功率激光治疗药物普遍存在但机制并不完全理解。已经表明,低功率激光吗辐照(LPLI)可以诱导光化学反应,激活细胞内信号通路。被认为是关键的二级信使吗由LPLI生产。通路由ROS的刺激LPLI。ROS和可以通过氧化事件被激活。使用Src记者基于荧光共振能量转移(FRET)和共焦激光扫描显微镜,我们可视化动态Src立即激活在海拉细胞LPLI之后。剂量依赖性的方式。磷酸化Tyr416检测到西方印迹。过氧化氢酶和单独或组合超氧化物歧化酶(SOD)、Src的激活由LPLI明显废除。PKC抑制剂Go6983加载,没有影响这种反应。外生H (2) O(2)也导致了Src的浓度激活。结果表明,这是ROS介导Src LPLI激活。可行性分析表明激光辐照低剂量(< / = 25 J /厘米(2))促进了海拉细胞生存能力,而高剂量受损。LPLI诱发ROS-mediated Src激活它可能发挥重要作用在biostimulatory吗LPLI的效果。

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