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Journal of Biochemistry Advance Access published online on May 7, 2008
Journal of Biochemistry, doi:10.1093/jb/mvn059
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© 2008 The Japanese Biochemical Society

Microglial cell death induced by glycated bovine serum albumin: nitric oxide involvement

Mohammad R. Khazaeia,b, Mehran Habibi-Rezaeia,*, Fereshteh Karimzadehb, Ali Akbar Moosavi-Movahedic, Abdo Alfattah Sarrafnejhadd, Farzaneh Sabounie and Mostafa Bakhtia

a School of Biology, College of Science, University of Tehran, Tehran, Iran.
b International Graduate Research School of Molecular Basis of Dynamic Cellular Processes, Westfaelische Wilhelmes-Universitaet, Muenster, Germany.
c Institute of Biochemistry and Biophysics, University of Tehran, Tehran, Iran.
d Department of Health, Medical Sciences, University of Tehran, Tehran, Iran
eNational Institute for Genetic Engineering and Biotechnology, Tehran, Iran.

*Corresponding author: Dr. Mehran Habibi-Rezaei. School of Biology, College of Science, University of Tehran, P.O. Box 14155-6455, Tehran, Iran. Fax: +98-21-66405141, E-mail address: mhabibi{at}khayam.ut.ac.ir

Received December 22, 2007; Accepted April 15, 2008


  Abstract

Nonenzymatic glycation results in the formation of Advanced Glycation End products (AGEs) through a nonenzymatic multi-step reaction of reducing sugars with proteins. AGEs have been suspected to be involved in the pathogenesis of several chronic clinical neurodegenerative complications including Alzheimer's disease, which is characterized with the activation of microglial cells in neuritic plaques. To find out the consequence of this activation on microglial cells we treated the cultured microglial cells with different glycation levels of Bovine Serum Albumin which were prepared in vitro. Extent of glycation of protein has been characterized during 16 weeks of incubation with glucose. Treatment of microglial cells with various levels of glycated albumin induced NO production and consequently cell death. We also tried to find out the mode of death in AGE-activated microglial cells. Altogether, our results suggest that AGE treatment causes microglia to undergo NO-mediated apoptotic and necrotic cell death in short term and long term, respectively. NO production is a consequence of iNOS expression in a JNK dependent RAGE signaling after activation of RAGE by AGE-BSA.

Key Words: nitric oxide, glycation, microglia, apoptosis, AGE


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