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

Cell Mol Life Sci. 2003 Jan;60(1):185-97. doi: 10.1007/s000180300013.

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.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Axons / metabolism
  • Axons / pathology*
  • Brain Stem / pathology
  • Encephalomyelitis, Autoimmune, Experimental / genetics*
  • Encephalomyelitis, Autoimmune, Experimental / metabolism
  • Encephalomyelitis, Autoimmune, Experimental / pathology*
  • Gene Expression
  • Growth Cones / pathology
  • Growth Substances / metabolism
  • Metallothionein / deficiency*
  • Metallothionein / genetics
  • Mice
  • Mice, Knockout
  • Nerve Growth Factors / metabolism
  • Oligodendroglia / pathology
  • Spinal Cord / pathology

Substances

  • Growth Substances
  • Nerve Growth Factors
  • Metallothionein