Bcl-2-expressing oligodendrocytes in multiple sclerosis lesions

Tanja Kuhlmann, Claudia Lucchinetti, Uwe K. Zettl, Andreas Bitsch, Hans Lassmann, Wolfgang Brück

Research output: Contribution to journalArticle

47 Scopus citations

Abstract

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system leading to selective destruction of myelin sheaths and/or oligodendrocytes. The immunological mechanisms responsible for myelin destruction and the primary target of the immune response have not yet been identified. Prior studies have reported a variable degree of oligodendrocyte preservation in actively demyelinating lesions. We have previously demonstrated that oligodendrocyte survival is heterogenous and varies between individual MS patients. Bcl-2 belongs to the group of apoptosis-associated proteins that protects cells from cell death. The purpose of the present study was to determine whether bcl-2 expression is associated with oligodendrocyte preservation observed in some early MS lesions. Double immunocytochemistry was performed with antibodies against bcl-2 and myelin oligodendrocyte glycoprotein (MOG) to identify bcl-2-expressing oligodendrocytes within MS lesions from 43 patients. The number of bcl-2-positive oligodendrocytes was determined depending on the lesion demyelinating activity and the disease course of the patients. The number of bcl-2-expressing oligodendrocytes increased within demyelinating lesions compared to the periplaque white matter, with highest numbers in remyelinating lesions. There was a significant association between the presence of bcl-2-positive oligodendrocytes and the presence of remyelination. The highest proportion of bcl-2-positive oligodendrocytes was observed in a subgroup of patients with relapsing-remitting disease course. The expression of apoptosis-associated proteins may contribute to oligodendrocyte preservation or loss in MS lesions.

Original languageEnglish (US)
Pages (from-to)34-39
Number of pages6
JournalGlia
Volume28
Issue number1
DOIs
StatePublished - Jan 1 1999

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Keywords

  • Apoptosis
  • Bcl-2
  • Multiple sclerosis
  • Oligodendrocytes

ASJC Scopus subject areas

  • Neurology
  • Cellular and Molecular Neuroscience

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