Abstract.
Metallothioneins I+II (MT-I+II) are antioxidant, neuroprotective factors. We previously showed that MT-I+II deficiency during experimental autoimmune encephalomyelitis (EAE) leads to increased disease incidence and clinical symptoms. Moreover, the inflammatory response of macrophages and T cells, oxidative stress, and apoptotic cell death during EAE were increased by MT-I+II deficiency. We now show for the first time that demyelination and axonal damage are significantly increased in MT-I+II deficient mice during EAE. Furthermore, oligodendroglial regeneration, growth cone formation, and tissue repair including expression of trophic factors were significantly reduced in MT-I+II-deficient mice during EAE. Accordingly, MT-I+II have protective and regenerative roles in the brain.
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Received 31 October 2002; received after revision 23 November 2002; accepted 26 November 2002
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ID="*"Corresponding author. M. Penkowa and C. Espejo contributed equally to this paper.
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Penkowa, M., Espejo, C., Martínez-Cáceres, E. et al. Increased demyelination and axonal damage in metallothionein I+II-deficient mice during experimental autoimmune encephalomyelitis. CMLS, Cell. Mol. Life Sci. 60, 185–197 (2003). https://doi.org/10.1007/s000180300013
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DOI: https://doi.org/10.1007/s000180300013