Document Type : Original Article
Stem Cells and Developmental Biology Department, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran
Genetics Department, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran
Medical Genetics Department, National Institute for Genetic Engineering and Biotechnology, Tehran, Iran
Developmetal Biology Department, University of Science and Culture, ACECR, Tehran, Iran
Physiology and Proteomics Department , Agricultural Biotechnology Research Institute of Iran, Karaj, Iran
Objective: Detection of central nervous system (CNS) molecular defects in an animal model of multiple sclerosis.
Materials and Methods: Experimental autoimmune encephalomyelitis (EAE) was induced by a myelin oligodendrocyte glycoprotein. Protein expression profiles in the central nervous system between healthy clinical scores 1 and 3 of EAE were studied using a two dimensional electrophoresis based proteomics approach coupled with MALDI TOF/TOF mass spectrometry. Results: We identified 8 mitochondrial proteins that were differentially expressed in CNS, all of them down-regulated in scores 1 and/or 3. Of these, 5 proteins belong to the mitochondrial respiratory chain including: NADH dehydrogenase (ubiquinone) Fe-S protein 8, cytochrome c oxidase Va, cytochrome c oxidase Vb, ATP5B, NADH dehydrogenase (ubiquinone) flavoprotein 2. 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 that hypoxia-like tissue injury in multiple sclerosis (MS) lesions may be due to mitochondrial impairment.