Role of galectin-3 in prion infections of the CNS

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...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2007-08, Vol.359 (3), p.672-678
Main Authors: Mok, Simon W.F., Riemer, Constanze, Madela, Kazimierz, Hsu, Daniel K., Liu, Fu-Tong, Gültner, Sandra, Heise, Ines, Baier, Michael
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
ABLATION
Animals
Astrocytosis
Atg5
Autophagy
Beclin-1
BRAIN
DEPOSITION
DOUBLE LABELLING
Endo/lysosomal activation
Galectin 3 - deficiency
Galectin 3 - genetics
Galectin 3 - metabolism
Galectin-3
Gene Expression Regulation
GENE REGULATION
Immunohistochemistry
INFLAMMATION
LAMP-2
Lysosomal-Associated Membrane Protein 2 - metabolism
MICE
Mice, Inbred C57BL
Mice, Knockout
Microgliosis
Prion
Prion Diseases - genetics
Prion Diseases - metabolism
Prion Diseases - pathology
PROTEINS
Scrapie
Survival Rate
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Summary: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.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2007.05.163