| First Author | Mok SW | Year | 2007 |
| Journal | Biochem Biophys Res Commun | Volume | 359 |
| Issue | 3 | Pages | 672-8 |
| PubMed ID | 17555713 | Mgi Jnum | J:122388 |
| Mgi Id | MGI:3714222 | Doi | 10.1016/j.bbrc.2007.05.163 |
| Citation | Mok SW, et al. (2007) Role of galectin-3 in prion infections of the CNS. Biochem Biophys Res Commun 359(3):672-8 |
| abstractText | 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. |
