Cell Journal (Jan 2009)

Central Nervous System Proteomics in Animal Model of Multiple Sclerosis Revealed Down-Regulation of Mithochondrial Proteins

  • Abolhassan Shahzadeh Fazeli,
  • Mohammad Hossein Sanati,
  • Davood Nasrabadi,
  • Alireza Pouya,
  • Hossein Baharvand,
  • Ghasem Hosseini Salekdeh

Journal volume & issue
Vol. 11, no. 2
pp. 236 – 243

Abstract

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Objective: Detection of central nervous system (CNS) molecular defects in an animal modelof multiple sclerosis.Materials and Methods: Experimental autoimmune encephalomyelitis (EAE) was inducedby a myelin oligodendrocyte glycoprotein. Protein expression profiles in the central nervoussystem between healthy clinical scores 1 and 3 of EAE were studied using a two dimensionalelectrophoresis based proteomics approach coupled with MALDI TOF/TOF massspectrometry.Results: We identified 8 mitochondrial proteins that were differentially expressed in CNS, allof them down-regulated in scores 1 and/or 3. Of these, 5 proteins belong to the mitochondrialrespiratory chain including: NADH dehydrogenase (ubiquinone) Fe-S protein 8, cytochromec oxidase Va, cytochrome c oxidase Vb, ATP5B, NADH dehydrogenase (ubiquinone) flavoprotein2. We also observed down-regulation of three other mitochondrial proteins including:glutaredoxin 5, estradiol 17 beta-dehydrogenase 8 and isocitrate dehydrogenase.Conclusion: Down-regulation of mitochondrial proteins supported the hypothesis thathypoxia-like tissue injury in multiple sclerosis (MS) lesions may be due to mitochondrialimpairment.

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