Increased demyelination and axonal damage in metallothionein I+II-deficient mice during experimental autoimmune encephalomyelitis |
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Authors: | M Penkowa C Espejo E M Martínez-Cáceres X Montalban J Hidalgo |
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Institution: | (1) Department of Medical Anatomy, The Panum Institute, University of Copenhagen, 2200, Copenhagen (Denmark), DK;(2) Unitat de Neuroimmunologia Clínica, Hospital Universitari Vall d'Hebron, 08035 Barcelona (Spain), ES;(3) Laboratory of Immunobiology for Research and Diagnostic Applications (LIRAD), Transfusion Center and Tissue Bank (CTBT), Barcelona (Spain), ES;(4) Institute of Neurosciences and Department of Cellular Biology, Physiology and Immunology, Autonomous University of Barcelona, Bellaterra, 08193 Barcelona (Spain), Fax: + 34 93 5812390, e-mail: juan.hidalgo@uab.es, ES |
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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.
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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Keywords: | , Metallothionein, EAE/MS, demyelination, neurodegeneration, regeneration, neurotrophic factor, |
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