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Galectin-1 and galectin-3 as key molecules for peripheral nerve degeneration and regeneration

1 Diabetic Neuropathy Project, Department of Sensory and Motor Systems, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan
2 Department of Biotechnology, Maebashi Institute of Technology, Maebashi, Gunma 371-0816, Japan
3 Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan
4 TechnoMaster Co. Ltd., Yokohama 236-0038, Japan

Shizuka Takaku and Naoko Niimi contributed equally to this work.

Topical Section: Lectins

There is growing evidence that galectin-1 (GAL-1) and galectin-3 (GAL-3) are involved in the process of axonal regeneration after injury and the pathogenesis of peripheral neuropathies, but the precise roles of these galectins in the peripheral nervous system (PNS) remain unclear. In this paper, we summarized the distribution and possible functions of GAL-1 and GAL-3 in the PNS at mature stages under normal and pathological conditions. Predominant expression of GAL-1 and GAL-3 in isolectin B4 (IB4)-binding small non-peptidergic sensory neurons in dorsal root ganglia (DRG) accords with the involvement of these molecules in nociceptive and thermoceptive functions and GDNF-induced neurite outgrowth. Up-regulation of GAL-1 mRNA/protein in the neurons and Schwann cells upon peripheral nerve injury suggests its active participation in axonal regeneration; both GAL-1 in the reduced and oxidized forms appear to be key molecules for normal onset of Wallerian degeneration and subsequent neurite outgrowth, but the latter lacks lectin activity and may promote the process by stimulating macrophages rather than directly acting on neurons. GAL-3 deficient mice exhibited the acceleration in the process of Wallerian degeneration, but there is room for argument on its pathological roles in axonal regeneration. Up-regulation of GAL-3 protein in immortalized Schwann cells IFRS1 under diabetic conditions and its cytoprotective functions on the cells suggest that it may act as a factor against the progression of diabetic neuropathy, but further evidence is needed to support this idea. All these findings have shed light on both physiological and pathological roles of GAL-1 and GAL-3 in the PNS, and further evidence will be helpful to develop novel strategies for functional restoration after peripheral nerve injury and therapeutic efficacy against diabetic and other neuropathies.
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