Abstract
Galectin-1 (Gal1) was the first identified member of the galectin family of β-galactosidase-binding proteins. Gal1 has important roles in processes fundamental to growth and survival of an organism, including cell adhesion, cell proliferation and apoptosis, and is expressed in many tissues, including the nervous system. In the 1980s, research focused on the developmental regulation of Gal1 expression during neurogenesis. Gal1 was found to be expressed mainly in peripherally-projecting neurons beginning early in neurogenesis, and its expression is maintained at high levels in subpopulations of these neurons in the adult rodent. Although the expression pattern of Gal1 implied that it may be involved in axonal guidance or targeting of subsets of sensory and motoneurons, possible roles of Gal1 in the nervous system had not been confirmed until recently. Gal1 has since been shown to be required for the proper guidance of subsets of primary olfactory axons (to targets in the olfactory bulb) and of primary somatosensory axons (to targets in the superficial dorsal horn). In addition, Gal1 has been implicated in the regenerative response of axons following peripheral nerve injury. Gal1 has been shown to promote axonal regeneration through the activation of macrophages. Also, Gal1 may act within the injured neuron to enhance regrowth: the injury-induced regulation of Gal1 in numerous types of peripherally- and centrally-projecting neurons correlates positively with the regenerative potential of their axons. In this review, we discuss the expression pattern of Gal1 in sensory and motoneurons, and the potential roles of Gal1 in development, axonal regeneration and neuropathic pain.
Keywords: drg, rhizotomy, axotomy, rl, axonal regeneration, neuropathic pain
Current Drug Targets
Title: Expression and Functions of Galectin-1 in Sensory and Motoneurons
Volume: 6 Issue: 4
Author(s): A. D. Gaudet, J. D. Steeves, W. Tetzlaff and M. S. Ramer
Affiliation:
Keywords: drg, rhizotomy, axotomy, rl, axonal regeneration, neuropathic pain
Abstract: Galectin-1 (Gal1) was the first identified member of the galectin family of β-galactosidase-binding proteins. Gal1 has important roles in processes fundamental to growth and survival of an organism, including cell adhesion, cell proliferation and apoptosis, and is expressed in many tissues, including the nervous system. In the 1980s, research focused on the developmental regulation of Gal1 expression during neurogenesis. Gal1 was found to be expressed mainly in peripherally-projecting neurons beginning early in neurogenesis, and its expression is maintained at high levels in subpopulations of these neurons in the adult rodent. Although the expression pattern of Gal1 implied that it may be involved in axonal guidance or targeting of subsets of sensory and motoneurons, possible roles of Gal1 in the nervous system had not been confirmed until recently. Gal1 has since been shown to be required for the proper guidance of subsets of primary olfactory axons (to targets in the olfactory bulb) and of primary somatosensory axons (to targets in the superficial dorsal horn). In addition, Gal1 has been implicated in the regenerative response of axons following peripheral nerve injury. Gal1 has been shown to promote axonal regeneration through the activation of macrophages. Also, Gal1 may act within the injured neuron to enhance regrowth: the injury-induced regulation of Gal1 in numerous types of peripherally- and centrally-projecting neurons correlates positively with the regenerative potential of their axons. In this review, we discuss the expression pattern of Gal1 in sensory and motoneurons, and the potential roles of Gal1 in development, axonal regeneration and neuropathic pain.
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Gaudet D. A., Steeves D. J., Tetzlaff W. and Ramer S. M., Expression and Functions of Galectin-1 in Sensory and Motoneurons, Current Drug Targets 2005; 6 (4) . https://dx.doi.org/10.2174/1389450054021864
DOI https://dx.doi.org/10.2174/1389450054021864 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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