Mok SWF, Riemer C, Madela K, Hsu DK, Liu FT, Gültner S, Heise I, Baier M (2007): Role of galectin-3 in prion infections of the CNS
Biochem. Biophys. Res. Com. 359 (3): 672-678.

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. Immunofluorescense 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.