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Galectins, (re)myelination and multiple sclerosis pathology

28 March 2012

PhD ceremony: Ms. M. Stancic, 14.30 uur, Academiegebouw, Broerstraat 5, Groningen

Dissertation: Galectins, (re)myelination and multiple sclerosis pathology

Promotor(s): prof. D. Hoekstra

Faculty: Medical Sciences

Identification of environmental signals that regulate the behaviour of oligodendrocytes (OLG), i.e., cells that produce insulating myelin sheaths around axons, and corresponding receptors on the cell surface through which these signals act, is necessary to understand both normal OLG development and their behaviour in demyelinating diseases, such as multiple sclerosis (MS). The findings in this thesis point to a role of galectins, i.e., β-galactoside-binding proteins, in the interaction between cells of the central nervous system that are likely highly relevant to myelination and demyelination of axons. The discovery of galactin-4 as a novel neuronal regulator of the timing of myelination will add to an improved understanding of mechanisms of (re)myelination. A misbalance in galectin-4 expression and its release from neurons or the interaction of galectin-4 with different components of the extracellular matrix might be responsible for remyelination failure in MS. Roles of galectins-1, -2, -3, -4 and -8 in the regulation of glial cell viability, survival and proliferation are also described. Interestingly, expression of some of these galectins is upregulated in MS lesions, and evidence suggests that they are of potential importance for the pathological mechanisms underlying MS. Taken together, the studies presented in this thesis warrant further research on galectins as promising targets for MS treatment since they are both potent regulators of inflammatory processes and glia cell behaviour.

Last modified:13 March 2020 12.59 a.m.
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