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. 2018 Sep 12;12:297. doi: 10.3389/fncel.2018.00297

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Copyright © 2018 Thomas and Pasquini.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Extracellular Gal-3 drives OLG differentiation and (re)myelination: Gal-3 is expressed in microglial cells during remyelination, favoring an M2 microglial phenotype and, therefore, fostering myelin phagocytosis through TREM-2b phagocytic receptor and OLG differentiation probably by IGFR-1 pathway stimulation. In OPC (i), Gal-3 drives early process outgrowth through enhanced actin assembly and a decrease in Erk 1/2 activation, and later regulates OLG maturation (ii) by inducing Akt activation and inhibiting β-catenin degradation to increase MBP expression and promotes gelsolin release and actin cytoskeleton disassembly. Also, microglia-released Gal-3 induces OLG fate in neural stem cells. Finally, Gal-3 promotes neurite outgrowth but exerts both deleterious and protective effects on neuronal death in ischemic brain injury.