Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 53, Issue 7, Pages 1459-1467Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2012.08.003
Keywords
Apoptosis; Alzheimer disease; Amyloid beta peptide; GSK3 beta; beta-Catenin; Akt; Low-power laser irradiation; Free radicals
Funding
- National Basic Research Program of China [2011CB910402, 2010CB732602]
- Program for Changjiang Scholars and Innovative Research Team in University [IRT0829]
- National Natural Science Foundation of China [81101741, 31101028]
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Apoptosis induced by amyloid beta peptide (A beta) is thought to associate with the pathogenesis of Alzheimer disease (AD). Accumulating evidence shows that low-power laser irradiation (LPLI) is capable of reducing A beta-induced apoptosis. However, the underlying mechanisms remain unclear. In this study, we report a novel molecular mechanism by which LPLI attenuates A beta(25-35)-induced apoptosis through the Akt/GSK3 beta/beta-catenin pathway. We found that Akt activated by LPLI interacted with GSK3 beta and phosphorylated it on Ser9 in the presence of A beta(25-35), which resulted in the inhibition of GSK3 beta. Furthermore, LPLI increased the nuclear translocation of beta-catenin and enhanced its T cell factor/lymphocyte enhancer factor-dependent transcriptional activity via the Akt/GSK3 beta pathway to promote cell survival upon treatment with A beta(25-35). Our data demonstrate that LPLI has a prosurvival effect on A beta-induced apoptosis and may be an effective therapeutic strategy in treating AD by targeting GSK3 beta. (C) 2012 Elsevier Inc. All rights reserved.
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