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

  • H. C. Hoyos
  • Mariel Marder
  • R. Ulrich
  • V. Gudi
  • M. Stangel
  • G. A. Rabinovich
  • L. A. Pasquini
  • J. M. Pasquini
Chapter

Abstract

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(Lgals3/) and wild type (WT) mice were fed a diet containing 0.2 % CPZ w/w for 6 weeks, after which CPZ was withdrawn in order to allow remyelination.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+, TNFα+ 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.

Keywords

Galectin-3 Myelination Demyelination Remyelination Cuprizone Microglia Oligodendrocytes MMPs 

Abbreviations

MMPs

Matrix metalloproteinases

Gal-3

Galectin-3

Lgals3/

Gal-3-deficient

WT

Wild type

CPZ

Cuprizone

CRD

Carbohydrate-recognition domain

CNS

Central nervous system

OLG

Oligodendrocyte

EAE

Experimental Autoimmune Encephalomyelitis

CC

Corpus callosum

OPC

Oligodendrocyte precursor cells

MBP

Myelin basic protein

PBS

Phosphate buffered saline

PFA

Paraformaldehyde

SVZ

Subventricular zone

EM

Electron Microscopy

GFAP

Glial Fibrillary Acidic Protein

IOD

Integrated optical density

Copyright information

© Springer International Publishing Switzerland 2016

Authors and Affiliations

  • H. C. Hoyos
    • 1
    • 2
  • Mariel Marder
    • 1
    • 2
  • R. Ulrich
    • 3
  • V. Gudi
    • 4
    • 5
  • M. Stangel
    • 4
    • 5
  • G. A. Rabinovich
    • 6
    • 7
  • L. A. Pasquini
    • 1
    • 2
    • 8
  • J. M. Pasquini
    • 1
    • 2
    • 8
  1. 1.Department of Biological Chemistry, School of Pharmacy and BiochemistryInstitute of Chemistry and Biological Physical Chemistry (IQUIFIB)Buenos AiresArgentina
  2. 2.School of Pharmacy and BiochemistryUniversity of Buenos Aires and National Research Council (CONICET)Buenos AiresArgentina
  3. 3.Department of PathologyUniversity of Veterinary Medicine HannoverHannoverGermany
  4. 4.Department of NeurologyHannover Medical SchoolHannoverGermany
  5. 5.Center for System NeurosciencesHannoverGermany
  6. 6.Laboratory of ImmunopathologyInstitute of Biology and Experimental Medicine (IBYME; CONICET)Buenos AiresArgentina
  7. 7.Laboratory of Functional Glycomics, Department of Biological Chemistry, Faculty of Exact and Natural SciencesUniversity of Buenos AiresBuenos AiresArgentina
  8. 8.Dpto. de Qca BiolFFyB-UBABs asArgentina

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