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Proceedings Paper

Mitochondrial signaling pathway involved in cell apoptosis induced by high-fluence low-power laser irradiation
Author(s): Shengnan Wu; Da Xing
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Paper 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.

Paper Details

Date Published: 17 February 2011
PDF: 7 pages
Proc. SPIE 7887, Mechanisms for Low-Light Therapy VI, 78870C (17 February 2011); doi: 10.1117/12.874283
Show Author Affiliations
Shengnan Wu, South China Normal Univ. (China)
Da Xing, South China Normal Univ. (China)

Published in SPIE Proceedings Vol. 7887:
Mechanisms for Low-Light Therapy VI
Michael R. Hamblin; Ronald W. Waynant; Juanita Anders, Editor(s)

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