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Retracted: Treatment with metallothionein prevents demyelination and axonal damage and increases oligodendrocyte precursors and tissue repair during experimental autoimmune encephalomyelitis
Author(s) -
Penkowa Milena,
Hidalgo Juan
Publication year - 2003
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.10615
Subject(s) - experimental autoimmune encephalomyelitis , multiple sclerosis , neuroprotection , oligodendrocyte , encephalomyelitis , myelin , immunology , metallothionein , oxidative stress , regeneration (biology) , inflammation , nerve growth factor , demyelinating disease , neurotrophin , medicine , central nervous system , pathology , biology , endocrinology , microbiology and biotechnology , receptor , biochemistry , gene
Experimental autoimmune encephalomyelitis (EAE) is an animal model for the human demyelinating disease multiple sclerosis (MS). EAE and MS are characterized by significant inflammation, demyelination, neuroglial damage, and cell death. Metallothionein‐I and ‐II (MT‐I + II) are antiinflammatory and neuroprotective proteins that are expressed during EAE and MS. We have shown recently that exogenous administration of Zn‐MT‐II to Lewis rats with EAE significantly reduced clinical symptoms and the inflammatory response, oxidative stress, and apoptosis of the infiltrated central nervous system areas. We show for the first time that Zn‐MT‐II treatment during EAE significantly prevents demyelination and axonal damage and transection, and stimulates oligodendroglial regeneration from precursor cells, as well as the expression of the growth factors basic fibroblast growth factor (bFGF), transforming growth factor (TGF)β, neurotrophin‐3 (NT‐3), NT‐4/5, and nerve growth factor (NGF). These beneficial effects of Zn‐MT‐II treatment could not be attributable to its zinc content per se. The present results support further the use of Zn‐MT‐II as a safe and successful therapy for multiple sclerosis. © 2003 Wiley‐Liss, Inc.