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The emerging role of galectins in (re)myelination and its potential for developing new approaches to treat multiple sclerosis.

Abstract

Multiple sclerosis (MS) is an inflammatory, demyelinating and neurodegenerative disease of the central nervous system with unknown etiology. Currently approved disease-modifying treatment modalities are immunomodulatory or immunosuppressive. While the applied drugs reduce the frequency and severity of the attacks, their efficacy to regenerate myelin membranes and to halt disease progression is limited. To achieve such therapeutic aims, understanding biological mechanisms of remyelination and identifying factors that interfere with remyelination in MS can give respective directions. Such a perspective is given by the emerging functional profile of galectins. They form a family of tissue lectins, which are potent effectors in processes as diverse as adhesion, apoptosis, immune mediator release or migration. This review focuses on endogenous and exogenous roles of galectins in glial cells such as oligodendrocytes, astrocytes and microglia in the context of de- and (re)myelination and its dysregulation in MS. Evidence is arising for a cooperation among family members so that timed expression and/or secretion of galectins-1, -3 and -4 result in modifying developmental myelination, (neuro)inflammatory processes, de- and remyelination. Dissecting the mechanisms that underlie the distinct activities of galectins and identifying galectins as target or tool to modulate remyelination have the potential to contribute to the development of novel therapeutic strategies for MS.

Authors+Show Affiliations

Department of Biomedical Sciences of Cells & Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, A. Deusinglaan 1, 9713 AV, Groningen, The Netherlands.Institute of Physiological Chemistry, Faculty of Veterinary Medicine, Ludwig-Maximilians-University Munich, Munich, Germany.Department of Biomedical Sciences of Cells & Systems, Section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, A. Deusinglaan 1, 9713 AV, Groningen, The Netherlands. w.baron@umcg.nl.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

31628495

Citation

de Jong, Charlotte G H M., et al. "The Emerging Role of Galectins in (re)myelination and Its Potential for Developing New Approaches to Treat Multiple Sclerosis." Cellular and Molecular Life Sciences : CMLS, 2019.
de Jong CGHM, Gabius HJ, Baron W. The emerging role of galectins in (re)myelination and its potential for developing new approaches to treat multiple sclerosis. Cell Mol Life Sci. 2019.
de Jong, C. G. H. M., Gabius, H. J., & Baron, W. (2019). The emerging role of galectins in (re)myelination and its potential for developing new approaches to treat multiple sclerosis. Cellular and Molecular Life Sciences : CMLS, doi:10.1007/s00018-019-03327-7.
de Jong CGHM, Gabius HJ, Baron W. The Emerging Role of Galectins in (re)myelination and Its Potential for Developing New Approaches to Treat Multiple Sclerosis. Cell Mol Life Sci. 2019 Oct 18; PubMed PMID: 31628495.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The emerging role of galectins in (re)myelination and its potential for developing new approaches to treat multiple sclerosis. AU - de Jong,Charlotte G H M, AU - Gabius,Hans-Joachim, AU - Baron,Wia, Y1 - 2019/10/18/ PY - 2019/07/13/received PY - 2019/09/30/accepted PY - 2019/09/27/revised PY - 2019/10/20/entrez KW - Galectins KW - Multiple sclerosis KW - Myelination KW - Oligodendrocytes KW - Remyelination JF - Cellular and molecular life sciences : CMLS JO - Cell. Mol. Life Sci. N2 - Multiple sclerosis (MS) is an inflammatory, demyelinating and neurodegenerative disease of the central nervous system with unknown etiology. Currently approved disease-modifying treatment modalities are immunomodulatory or immunosuppressive. While the applied drugs reduce the frequency and severity of the attacks, their efficacy to regenerate myelin membranes and to halt disease progression is limited. To achieve such therapeutic aims, understanding biological mechanisms of remyelination and identifying factors that interfere with remyelination in MS can give respective directions. Such a perspective is given by the emerging functional profile of galectins. They form a family of tissue lectins, which are potent effectors in processes as diverse as adhesion, apoptosis, immune mediator release or migration. This review focuses on endogenous and exogenous roles of galectins in glial cells such as oligodendrocytes, astrocytes and microglia in the context of de- and (re)myelination and its dysregulation in MS. Evidence is arising for a cooperation among family members so that timed expression and/or secretion of galectins-1, -3 and -4 result in modifying developmental myelination, (neuro)inflammatory processes, de- and remyelination. Dissecting the mechanisms that underlie the distinct activities of galectins and identifying galectins as target or tool to modulate remyelination have the potential to contribute to the development of novel therapeutic strategies for MS. SN - 1420-9071 UR - https://www.unboundmedicine.com/medline/citation/31628495/The_emerging_role_of_galectins_in_(re)myelination_and_its_potential_for_developing_new_approaches_to_treat_multiple_sclerosis L2 - https://dx.doi.org/10.1007/s00018-019-03327-7 DB - PRIME DP - Unbound Medicine ER -