The role of galectin-3: from oligodendroglial differentiation and myelination to demyelination and remyelination processes in a cuprizone-induced demyelination model.

H.C. HOYOS; M. MARDER; R. ULRICH, ; V. GUDI; M. STANGEL; G.A. RABINOVICH; L.A. PASQUINI; J.M. PASQUINI

ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY.

SPRINGER-VERLAG BERLIN

Año: 2016 vol. 949 p. 331 - 332

0065-2598

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(Lgals3−/−) and wild type (WT) mice were fed a diet containing 0.2 % CPZ w/w for 6 weeks, after which CPZ was withdrawn in order to allow remyelination.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