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

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

Glial Cells in Health and Disease of the CNS

Springer

Año: 2016; p. 311 - 332

Theaim of the present work was to combine our previously published results withour new data to show how Galectin-3 controls myelin integrity and function, promotesoligodendroglial cell differentiation and regulates microglial responses to limitcuprizone (CPZ)-induced demyelination and foster remyelination. In this study,eight-week-old Lgals3-/-and wild type (WT) mice were fed a diet containing 0.2% CPZ w/w during 6 weeks,after which CPZ was withdrawn in order to allow remyelination. Our results showthat remyelination was less efficient in Lgals3-/-than in WT mice. Electron microscopy images from remyelinated sections in Lgals3-/- micerevealed collapsed axons with a defective myelin wrap, while remyelinated WTmice showed normal axons without any relevant myelin wrap disruption. Anincrease in MMP-3 expression was found during remyelination in WT but not in Lgals3-/- mice. Results also showeda significant decrease in the number of CD45+, TNFa+ and TREM-2b+cells in WT mice only, with no alterations in Lgals3-/- mice alongthe demyelination-remyelination process. Therefore, Gal-3 influences theremyelination process through mechanisms involving the tuning of microglialcells, modulation of MMP activity and changes in myelin architecture.