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The reactive oxygen species–Src–Stat3 pathway provokes negative feedback inhibition of apoptosis induced by high‐fluence low‐power laser irradiation
Author(s) -
Sun Xuegang,
Wu Shengnan,
Xing Da
Publication year - 2010
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2010.07884.x
Subject(s) - stat3 , apoptosis , reactive oxygen species , microbiology and biotechnology , stat protein , chemistry , signal transduction , oxidative stress , biology , biochemistry
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.