Involvement of neuropsin in the pathogenesis of experimental autoimmune encephalomyelitis

Ryuji Terayama, Yoshio Bando, Masahiro Yamada, Shigetaka Yoshida

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Inflammation, demyelination, and axonal damage of the central nervous system (CNS) are major pathological features of multiple sclerosis (MS). Proteolytic digestion of the blood-brain barrier and myelin protein by serine proteases is known to contribute to the development and progression of MS. Neuropsin, a serine protease, has a role in neuronal plasticity, and its expression has been shown to be upregulated in response to injury to the CNS. To determine the possible involvement of neuropsin in demyelinating diseases of the CNS, we examined its expression in myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), a recognized animal model for MS. Neuropsin mRNA expression was induced in the spinal cord white matter of mice with EAE. Combined in situ hybridization and immunohistochemistry demonstrated that most of the cells expressing neuropsin mRNA showed immunoreactivity for CNPase, a cell-specific marker for oligodendrocytes. Mice lacking neuropsin (neuropsin-/-) exhibited an altered EAE progression characterized by delayed onset and progression of clinical symptoms as compared to wild-type mice. Neuropsin-/- mice also showed attenuated demyelination and delayed oligodendroglial death early during the course of EAE. These observations suggest that neuropsin is involved in the pathogenesis of EAE mediated by demyelination and oligodendroglial death.

Original languageEnglish
Pages (from-to)108-118
Number of pages11
JournalGLIA
Volume52
Issue number2
DOIs
Publication statusPublished - Nov 1 2005
Externally publishedYes

Keywords

  • Demyelination
  • Multiple sclerosis
  • Oligodendrocytes
  • Serine protease

ASJC Scopus subject areas

  • Neurology
  • Cellular and Molecular Neuroscience

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