Role of galectin-3 in prion infections of the CNS

Simon W F Mok, Constanze Riemer, Kazimierz Madela, Daniel K. Hsu, Fu-Tong Liu, Sandra Gültner, Ines Heise, Michael Baier

Research output: Contribution to journalArticle

52 Scopus citations

Abstract

Galectin-3 is a multi-functional protein and participates in mediating inflammatory reactions. The pronounced overexpression of galectin-3 in prion-infected brain tissue prompted us to study the role of this protein in a murine prion model. Immunofluorescence double-labelling identified microglia as the major cell type expressing galectin-3. Ablation of galectin-3 did not affect PrPSc-deposition and development of gliosis. However, galectin-3-/--mice showed prolonged survival times upon intracerebral and peripheral scrapie infections. Moreover, protein levels of the lysosomal activation marker LAMP-2 were markedly reduced in prion-infected galectin-3-/--mice suggesting a role of galectin-3 in regulation of lysosomal functions. Lower mRNA levels of Beclin-1 and Atg5 in prion-infected wild-type and galectin-3-/--mice indicated an impairment of autophagy although autophagosome formation was unchanged. The results point towards a detrimental role of galectin-3 in prion infections of the CNS and suggest that endo-/lysosomal dysfunction in combination with reduced autophagy may contribute to disease development.

Original languageEnglish (US)
Pages (from-to)672-678
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume359
Issue number3
DOIs
StatePublished - Aug 3 2007

Keywords

  • Astrocytosis
  • Atg5
  • Autophagy
  • Beclin-1
  • Endo/lysosomal activation
  • Galectin-3
  • LAMP-2
  • Microgliosis
  • Prion
  • Scrapie

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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  • Cite this

    Mok, S. W. F., Riemer, C., Madela, K., Hsu, D. K., Liu, F-T., Gültner, S., Heise, I., & Baier, M. (2007). Role of galectin-3 in prion infections of the CNS. Biochemical and Biophysical Research Communications, 359(3), 672-678. https://doi.org/10.1016/j.bbrc.2007.05.163