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. 2021 Oct 15;15:767330. doi: 10.3389/fnana.2021.767330

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Copyright © 2021 Nio-Kobayashi and Itabashi.

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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Galectins in neurite outgrowth and branching (A) as well as (re)myelination (B). Galectin-1 from astrocytes and galectin-3 from activated microglia promote neurite outgrowth and branching, by blocking Semaphorin 3A (Sema3A) pathway or binding to neural cell adhesion molecule L1 (NCAML1) and laminin, respectively (A). Galectin-4 is segmentary localized to the axon by binding to sulfatide and NCAML1, regulating axonal growth and branching (A). Oxidization and phosphorylation of galectin-1 and galectin-3, respectively, enhances neuroprotective activities of them (A). In damaged neurons, galectin-3 from M1 type microglia enhances inflammation, whereas galectin-3 from M2 type microglia promotes phagocytic cleaning and oligodendrocyte differentiation (B). Galectin-1, possibly from astrocytes, induces shift from the M1 to M2 phenotype of activated microglia and oligodendrocyte differentiation. Galectin-4 from regenerating axon inhibits maturation of pre-myelinating oligodendrocyte to determine the timing of (re)myelination.