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Submitted on January 18, 2006
Accepted on October 31, 2006
Department of Neurology, Department of Mechanical Engineering and Department of Biomedical Engineering, Department of Civil and Environmental Engineering, University of Michigan, Ann Arbor, Michigan
* To whom correspondence should be addressed. E-mail: andreav{at}umich.edu.
The receptor for advanced glycation end-products (RAGE) may promote diabetic vascular and renal disease through the activation of intracellular signaling pathways that promote oxidative stress. Oxidative stress is a mediator of hyperglycemia-induced cell injury and a unifying theme for all mechanisms of diabetic complications, but there are few studies on the expression and potential contribution of RAGE in diabetic neuropathy. The current study demonstrates that dorsal root ganglia (DRG) neurons express functional RAGE and respond to the RAGE ligand S100 with similar downstream signaling, oxidative stress, and cellular injury as other diabetic complication-prone tissues. RAGE-induced PI-3K activity is associated with formation of reactive oxygen species (ROS), caspase 3 activation, and nuclear DNA degradation. These events are prevented by treatment with the antioxidant 
-lipoic acid. Our data indicate that therapies aimed at decreasing RAGE ligands, blocking RAGE signaling, or preventing oxidative stress could significantly decrease the development of neuropathy in diabetic patients.
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