Increased demyelination and axonal damage in metallothionein I+II-deficient mice during experimental autoimmune encephalomyelitis

被引:27
|
作者
Penkowa, M
Espejo, C
Martínez-Caceres, EM
Montalban, X
Hidalgo, J [1 ]
机构
[1] Autonomous Univ Barcelona, Inst Neurosci, E-08193 Barcelona, Spain
[2] Autonomous Univ Barcelona, Dept Cellular Biol Physiol & Immunol, E-08193 Barcelona, Spain
[3] Univ Copenhagen, Panum Inst, Dept Med Anat, DK-2200 Copenhagen, Denmark
[4] Univ Barcelona, Hosp Gen Valle Hebron, Unitat Neuroimmunol Clin, Barcelona 08035, Spain
[5] CTBT, LIRAD, Barcelona, Spain
关键词
metallothionein; EAE/MS; demyelination; neurodegeneration; regeneration; neurotrophic factor;
D O I
10.1007/s000180300013
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:185 / 197
页数:13
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