Galectin-1 in regenerating motoneurons

Authors

  • J. McGraw,

    1. ICORD (International Collaboration On Repair Discoveries), 6270 University Boulevard, University of British Columbia, Vancouver, Canada, V6T 1Z4
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  • L. T. McPhail,

    1. ICORD (International Collaboration On Repair Discoveries), 6270 University Boulevard, University of British Columbia, Vancouver, Canada, V6T 1Z4
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  • L. W. Oschipok,

    1. ICORD (International Collaboration On Repair Discoveries), 6270 University Boulevard, University of British Columbia, Vancouver, Canada, V6T 1Z4
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  • H. Horie,

    1. Advanced Research Center Biological Sciences, Waseda University, Nishitokyo, Japan
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  • F. Poirier,

    1. Departement de Biologie du Developpement, Institut Jacques Monod, Paris, France
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  • J. D. Steeves,

    1. ICORD (International Collaboration On Repair Discoveries), 6270 University Boulevard, University of British Columbia, Vancouver, Canada, V6T 1Z4
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  • M. S. Ramer,

    1. ICORD (International Collaboration On Repair Discoveries), 6270 University Boulevard, University of British Columbia, Vancouver, Canada, V6T 1Z4
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    • M.S.R. and W.T. contributed equally to the work.

  • W. Tetzlaff

    1. ICORD (International Collaboration On Repair Discoveries), 6270 University Boulevard, University of British Columbia, Vancouver, Canada, V6T 1Z4
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    • M.S.R. and W.T. contributed equally to the work.


Dr W. Tetzlaff, as above.
E-mail: tetzlaff@icord.org

Abstract

The exogenous application of recombinant galectin-1 has recently been shown to promote the rate of peripheral nerve regeneration. Endogenous neuronal galectin-1 expression has recently been demonstrated to increase after axotomy. Here we demonstrate a significant increase in the endogenous neuronal expression of galectin-1 mRNA in facial motoneurons after either a nerve resection or crush injury in mice. This increase in galectin-1 expression was due in part to the loss of target-derived factor(s) as indicated by both the return of galectin-1 expression to control levels following target re-innervation and the increase in galectin-1 expression after blockade of axonal transport by an interneuronal colchicine injection. Furthermore, interneuronal injections of glial-derived neurotrophic factor into the uninjured nerve also increased galectin-1 mRNA expression within facial motoneurons suggesting that positive signals may also be involved in the regulation of galectin-1 expression. Galectin-1 null mutant mice showed an attenuated rate of functional recovery of whisking movement after a facial nerve crush.

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