These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: The reactive oxygen species-Src-Stat3 pathway provokes negative feedback inhibition of apoptosis induced by high-fluence low-power laser irradiation.
    Author: Sun X, Wu S, Xing D.
    Journal: FEBS J; 2010 Nov; 277(22):4789-802. PubMed ID: 20977672.
    Abstract:
    High-fluence low-power laser irradiation (HF-LPLI) can induce apoptosis by triggering mitochondrial oxidative stress. Signal transducer and activator of transcription 3 (Stat3) is an important transcription factor in the modulation of cell proliferation and apoptosis. Here, using real-time single-cell analysis and western blotting analysis, we investigated the changes in activities of Stat3 in COS-7 cells upon HF-LPLI (633 nm, 80 and 120 J·cm(-2)) and the underlying mechanisms involved. We found that Stat3 was significantly activated by HF-LPLI in a time-dependent and dose-dependent manner. Stat3 activation attenuated HF-LPLI-induced apoptosis, as shown by the fact that both dominant negative Stat3 (Y705F) and Stat3 small interfering RNA expression enhanced cellular apoptosis induced by HF-LPLI. Moreover, we also found that Src kinase was the major positive regulator of Stat3 activation induced by HF-LPLI. Reactive oxygen species (ROS) generation was essential for Stat3 and Src activation upon HF-LPLI, because scavenging of ROS by vitamin C or N-acetylcysteine totally abrogated the activation of Stat3 and Src. Taken together, these findings show that the ROS-Src-Stat3 pathway mediates a negative feedback inhibition of apoptosis induced by HF-LPLI in COS-7 cells. Our research will provide new insights into the mechanism of apoptosis caused by HF-LPLI, and also extend the functional study of Stat3.
    [Abstract] [Full Text] [Related] [New Search]