The Role of Galectin-3: From Oligodendroglial Differentiation and Myelination to Demyelination and Remyelination Processes in a Cuprizone-Induced Demyelination Model

HOYOS H; PASQUINI LA

ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY.

SPRINGER-VERLAG BERLIN

Año: 2016

0065-2598

The aim of this work was to combine our previously published resultswith our new data to show how galectin-3 (Gal-3) controls myelin integrity andfunction, promotes oligodendroglial cell differentiation, and regulates microglialresponses to limit cuprizone- (CPZ)-induced demyelination and foster remyelination.In this study, 8-week-old Gal-3-deficient (Lgals3−/−) and wild type (WT) micewere fed a diet containing 0.2 % CPZ w/w for 6 weeks, after which CPZ waswithdrawn in order to allow remyelination. Our results show that remyelination wasless efficient in Lgals3−/− than in WT mice. Electron microscopic images fromremyelinated sections in Lgals3−/− mice revealed collapsed axons with a defectivemyelin wrap, while remyelinated WT mice had normal axons without relevantmyelin wrap disruption. MMP-3 expression increased during remyelination in WTbut not in Lgals3−/− mice. The number of CD45+, TNFa+ and TREM-2b+ cellsdecreased only in WT mice only, with no alterations in Lgals3−/− mice duringdemyelination and remyelination. Therefore, Gal-3 influences remyelination by mechanisms involving the tuning of microglial cells, modulation of MMP activity,and changes in myelin architecture.