Expression of Golli proteins in adult human brain and multiple sclerosis lesions

J Neuroimmunol. 2002 Jun;127(1-2):1-12. doi: 10.1016/s0165-5728(02)00070-x.

Abstract

It has been suggested that Golli proteins, structurally related to myelin basic proteins (MBPs), have a role in autoimmune processes. We studied the expression of these proteins in multiple sclerosis (MS) and determined that the number of Golli-immunoreactive (ir) cells was significantly higher around lesions of chronic MS than in control white matter. Golli proteins were expressed in the adult oligodendrocyte precursor cells (OPCs), activated microglia/macrophages, and some demyelinated axons around MS lesions. Their expression in adult OPCs indicates remyelination attempts, whereas the expression in the subpopulation of microglia/macrophages suggests roles in the immune processes of MS. In addition, Golli proteins may be markers of axonal transection, which is characteristic for MS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Adult
  • Aged
  • Aged, 80 and over
  • Brain / immunology
  • Brain / pathology*
  • Brain Chemistry*
  • Chronic Disease
  • Female
  • Humans
  • Immunohistochemistry
  • Macrophages / chemistry
  • Macrophages / metabolism
  • Macrophages / pathology
  • Male
  • Microglia / chemistry
  • Microglia / metabolism
  • Microglia / pathology
  • Middle Aged
  • Multiple Sclerosis / immunology
  • Multiple Sclerosis / metabolism*
  • Multiple Sclerosis / pathology
  • Myelin Basic Protein
  • Nerve Tissue Proteins / analysis*
  • Nerve Tissue Proteins / biosynthesis
  • Nerve Tissue Proteins / immunology
  • Oligodendroglia / chemistry
  • Oligodendroglia / metabolism
  • Oligodendroglia / pathology
  • Stem Cells / chemistry
  • Stem Cells / metabolism
  • Stem Cells / pathology
  • Transcription Factors / analysis*
  • Transcription Factors / biosynthesis
  • Transcription Factors / immunology

Substances

  • MBP protein, human
  • Myelin Basic Protein
  • Nerve Tissue Proteins
  • Transcription Factors