Role of Galectin-3 in Prion Infections of the Cns.
From: Project Neurodegenerative Diseases, Robert-Koch-Institut, Nordufer 20, 13353 Berlin, Germany.
Biochemical and biophysical research communications
- Publish Date: Aug 2007
- ISSN: 0006-291X
- Volume: 359
- Issue: 3
- Pages: 672-8
- Medium: Print
- Language: English
- Citation (JAMA): Mok Simon W F, Riemer Constanze, Madela Kazimierz, et al. Role of Galectin-3 in Prion Infections of the Cns.. Biochem. Biophys. Res. Commun. Aug 2007;359:672-8
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 PrP(Sc)-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.
Mesh Headings (Keywords): Animals, Autophagy, Galectin 3, Gene Expression Regulation, Immunohistochemistry, Lysosomal-Associated Membrane Protein 2, Mice, Mice, Inbred C57BL, Mice, Knockout, Prion Diseases, Survival Rate
Check for Full Text / PubMed Unique Identifier (PMID): 17555713
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