Microglial Cell Death Induced by Glycated Bovine Serum Albumin: Nitric Oxide Involvement
| Autor: | Farzaneh Sabouni, Mostafa Bakhti, Mehran Habibi-Rezaei, Mohammad Khazaei, Fereshteh Karimzadeh, Ali Akbar Moosavi-Movahedi, Abdo Alfattah Sarrafnejhad |
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| Rok vydání: | 2008 |
| Předmět: |
Glycation End Products
Advanced medicine.medical_specialty Programmed cell death Necrosis Cell Survival MAP Kinase Signaling System Receptor for Advanced Glycation End Products Nitric Oxide Synthase Type II Apoptosis Nitric Oxide Biochemistry RAGE (receptor) Glycation Internal medicine medicine Animals Glycated Serum Albumin Annexin A5 Rats Wistar Receptors Immunologic Bovine serum albumin Molecular Biology Cells Cultured Serum Albumin Microglia biology Chemistry JNK Mitogen-Activated Protein Kinases General Medicine Rats Nitric oxide synthase Endocrinology medicine.anatomical_structure Immunology biology.protein Cattle medicine.symptom |
| Zdroj: | The Journal of Biochemistry. 144:197-206 |
| ISSN: | 1756-2651 0021-924X |
| DOI: | 10.1093/jb/mvn059 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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