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Role of galectin-3 in prion infections of the CNS
Simon W F Mok1, Constanze Riemer, Kazimierz Madela
1Project Neurodegenerative Diseases, Robert-Koch-Institut, Nordufer 20, 13353 Berlin, Germany.
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.
Insights
Galectin-3 exacerbates prion disease in mice by impairing lysosomal function and autophagy. Removing galectin-3 (galectin-3 knockout) prolonged survival in prion-infected mice.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Galectin-3 is a protein involved in inflammatory responses.
- Galectin-3 is significantly overexpressed in prion-infected brain tissue.
Purpose of the Study:
- To investigate the role of galectin-3 in prion disease pathogenesis using a murine model.
- To determine the impact of galectin-3 ablation on prion disease progression and host survival.
Main Methods:
- Immunofluorescence double-labeling to identify galectin-3 expressing cells.
- Utilizing galectin-3 knockout (galectin-3(-/-)) mice for prion infection studies.
- Assessing PrP(Sc) deposition, gliosis, survival times, LAMP-2 levels, and autophagy markers (Beclin-1, Atg5).
Main Results:
- Microglia were identified as the primary galectin-3 expressing cells in prion-infected brains.
- Galectin-3 deficiency did not alter PrP(Sc) deposition or gliosis but significantly prolonged survival.
- Reduced LAMP-2 levels in knockout mice suggest impaired lysosomal function, while autophagy markers indicated impairment in both genotypes.
Conclusions:
- Galectin-3 plays a detrimental role in prion infections within the central nervous system.
- Galectin-3 contributes to disease development through endo-/lysosomal dysfunction and reduced autophagy.
- Targeting galectin-3 may offer a therapeutic strategy for prion diseases.
