17 February 2011 Mitochondrial signaling pathway involved in cell apoptosis induced by high-fluence low-power laser irradiation
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Proceedings Volume 7887, Mechanisms for Low-Light Therapy VI; 78870C (2011) https://doi.org/10.1117/12.874283
Event: SPIE BiOS, 2011, San Francisco, California, United States
Abstract
High fluence low-power laser irradiation (HF-LPLI) is a new stimulus to trigger cell apoptosis. Recently, great efforts have been made to investigate the mechanism involved in it. Our results show that HF-LPLI induces cell apoptosis through a large amount of intracellular reactive oxygen species (ROS), especially a higher generation in mitochondria. These triggered ROS causes mitochondrial injury manifested by mitochondrial depolarization and cytochrome c release. Caspase-3 activation is a downstream event which executed cell apoptosis finally. In addition, we exclude caspase-8/Bid signaling pathway in HF-LPLI-induced cell apoptosis. However, another important Bcl-2 pro-apoptotic member Bax participates in the apoptotic process. Our result show that Bax is activated after the diffusion of mitochondrial transmembrane potential and cytochrome c release, suggesting that Bax does not affect outer mitochondrial membrane permeabilization (OMMP). We postulate that the activation of Bax is mediated by oxidative stress caused by laser irradiation through ROS/GSK-3β/Bax pathway. Further studies need to be performed to clarify the exactly mechanism involved in HF-LPLI induced cell apoptosis.
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Shengnan Wu, Da Xing, "Mitochondrial signaling pathway involved in cell apoptosis induced by high-fluence low-power laser irradiation", Proc. SPIE 7887, Mechanisms for Low-Light Therapy VI, 78870C (17 February 2011); doi: 10.1117/12.874283; https://doi.org/10.1117/12.874283
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