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Journal of Biochemistry Advance Access originally published online on May 7, 2008
Journal of Biochemistry 2008 144(2):197-206; 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. Khazaei1,2, Mehran Habibi-Rezaei1,*, Fereshteh Karimzadeh2, Ali Akbar Moosavi-Movahedi3, Abdo Alfattah Sarrafnejhad4, Farzaneh Sabouni5 and Mostafa Bakhti1

1School of Biology, College of Science, University of Tehran, Tehran, Iran; 2International Graduate Research School of Molecular Basis of Dynamic Cellular Processes, Westfaelische Wilhelmes-Universitaet, Muenster, Germany; 3Institute of Biochemistry and Biophysics; 4Department of Health, Medical Sciences, University of Tehran; and 5National Institute for Genetic Engineering and Biotechnology, Tehran, Iran

*To whom correspondence should be addressed. Tel: +98-21-61113214, Fax: +98-21-66405141, E-mail: 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 multistep 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 (BSA) 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 nitric oxide (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 signalling after activation of RAGE by AGE–BSA.

Key Words: advanced glycation end products, apoptosis, glycation, microglia, nitric oxide


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