Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 39, Issue 6, Pages 823-831Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2005.05.014
Keywords
human primary oligodendrocytes; myelin gene expression; proinflammatory cytokines; reactive oxygen species
Funding
- NCRR NIH HHS [P20RR18759, P20 RR018759] Funding Source: Medline
- NINDS NIH HHS [R01 NS039940-05A1, NS39940, R01 NS039940] Funding Source: Medline
- CSR NIH HHS [RG3422AI/1] Funding Source: Medline
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Multiple sclerosis (MS) is a chronic autoimmune demyelinating disorder of the central nervous system (CNS) of unknown etiology. Several studies have shown that demyelination in MS is caused by proinflammatory mediators which are released by perivascular infiltrates and/or activated glial cells. To understand if proinfammatory mediators such as IL (interleukin)-1 beta and TNF (tumor necrosis factor)-alpha are capable of modulating the expression of myelin-specific genes, we investigated the effect of these cytokines on the expression of myelin basic protein (MBP), 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase), myelin oligodendrocyte glycoprotein (MOG), and proteolipid protein (PLP) in human primary oligodendrocytes. Interestingly, both IL-1 beta and TNF-alpha markedly inhibited the expression of MOG, CNPase, and PLP but not MBP, the effect that was blocked by antioxidants such as N-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC). Consistently, oxidants and prooxidants like H2O2 and diamide also markedly inhibited the expression of MOG, CNPase, and PLP. Furthermore, both IL-1 beta and TNF-alpha induced the production of H2O2. Taken together, these studies suggest that proinflammatory cytokines inhibit the expression of myelin genes in human primary oligodendrocytes through the alteration of cellular redox. (c) 2005 Elsevier Inc. All rights reserved.
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