Characteristics and mechanism of cell apoptosis induced by high fluence low-power laser irradiation

Shengnan Wu, Da Xing*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingConference contributionpeer-review

Abstract

High fluence low-power laser irradiation (LPLI) can induce cell apoptosis which is mediated by a high level of mitochondrial reactive oxygen species (ROS) production; however the mechanism is still unclear. Here, we further studied the mitochondrial signaling pathways involved in the apoptotic process. Activation of caspase-9 indicated an apoptotic process occurred under the high fluence LPLI treatment. Increasing of dichlorodihydrofluorescein diacetate (H2DCFDA) fluorescence products showed a high level of mitochondrial ROS generation after irradiation. Cyclosporine A (CsA) has been reported to inhibit some kinds of apoptosis, which are especially mediated by ROS. The question is whether CsA has some effect on high fluence LPLI induced apoptosis. Results showed that CsA significantly delayed mitochondria depolarization, observably delayed cell death in response to high fluence LPLI treatment demonstrating a significant protective role of CsA on the apoptotic process. These results suggest that high fluence LPLI induced cell apoptosis via some CsA-sensitive mitochondrial signal pathways.

Original languageEnglish
Title of host publicationBiophotonics and Immune Responses III
DOIs
Publication statusPublished - 2008
Externally publishedYes
EventBiophotonics and Immune Responses III - San Jose, CA, United States
Duration: 21 Jan 200821 Jan 2008

Publication series

NameProgress in Biomedical Optics and Imaging - Proceedings of SPIE
Volume6857
ISSN (Print)1605-7422

Conference

ConferenceBiophotonics and Immune Responses III
Country/TerritoryUnited States
CitySan Jose, CA
Period21/01/0821/01/08

Keywords

  • Apoptosis
  • Cyclosporine A (CsA)
  • Low power laser irradiation (LPLI)
  • Reactive oxygen species (ROS)

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