Expression of the endocytosis regulatory proteins Rab5 and Rabaptin-5 in glial cytoplasmic inclusions from brains with multiple system atrophy

Clin Neuropathol. 2000 Mar-Apr;19(2):51-6.

Abstract

Background: Glial cytoplasmic inclusions (GCIs) occur specifically in oligodendrocytes in brains with multiple system atrophy (MSA). Oligodendrocytes in MSA appear to be functionally altered in their nature in terms of the occurrence of GCIs and aberrant expression of various proteins such as neuron specific protein, MAP2 or pre-synaptic protein, ct-synuclein. The present study examined whether or not aberrant expression of the endocytosis regulatory proteins Rab5 and Rabaptin-5 occcur in oligodendrocytes of brains with MSA.

Materials and methods: We examined immunohistochemically the post-mortem brain tissues from 5 patients with MSA and 5 controls. Immunohistochemistry was done using monoclonal anti-Rab5 and anti-Rabaptin-5 antibodies based on ABC method.

Results: We have observed Rab5 and Rabaptin-5 immunoreactivity in the neuronal somata and axons of the controls, suggesting that Rab5 and Rabaptin-5 are involved in the regulation of the endocytosis in neurons of the human central nervous system. In the brain tissues from patients with MSA, we have found Rab5 and Rabaptin-5 immunoreactivity in GCIs.

Conclusion: Rab5, in association with Rabaptin-5, has been demonstrated in the early endosome and regulates the endocytosis. Since Rab5 and Rabaptin-5 have been immunolocalized to neurons in the human brains, we propose that oligodendrocytes may ectopically express Rab5 and Rabaptin-5 in MSA. Thus, the oligodendrocytes in MSA brains appear to be functionally significantly altered, which may be associated with the formation of GCIs in the oligodendrocytes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Brain / pathology*
  • Endocytosis / physiology*
  • Female
  • Humans
  • Immunoenzyme Techniques
  • Inclusion Bodies / pathology*
  • Male
  • Membrane Proteins / analysis*
  • Middle Aged
  • Oligodendroglia / pathology*
  • Olivopontocerebellar Atrophies / pathology*
  • Vesicular Transport Proteins*
  • rab5 GTP-Binding Proteins / analysis*

Substances

  • Membrane Proteins
  • RABEP1 protein, human
  • Vesicular Transport Proteins
  • rab5 GTP-Binding Proteins