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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.
AbstractList 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.
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.
Author McGraw, J.
Poirier, F.
Steeves, J. D.
Ramer, M. S.
Tetzlaff, W.
Horie, H.
McPhail, L. T.
Oschipok, L. W.
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  surname: McGraw
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  surname: McPhail
  fullname: McPhail, L. T.
  organization: ICORD (International Collaboration On Repair Discoveries), 6270 University Boulevard, University of British Columbia, Vancouver, Canada, V6T 1Z4
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  givenname: L. W.
  surname: Oschipok
  fullname: Oschipok, L. W.
  organization: ICORD (International Collaboration On Repair Discoveries), 6270 University Boulevard, University of British Columbia, Vancouver, Canada, V6T 1Z4
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  givenname: H.
  surname: Horie
  fullname: Horie, H.
  organization: Advanced Research Center Biological Sciences, Waseda University, Nishitokyo, Japan
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  surname: Poirier
  fullname: Poirier, F.
  organization: Departement de Biologie du Developpement, Institut Jacques Monod, Paris, France
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  surname: Ramer
  fullname: Ramer, M. S.
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  givenname: W.
  surname: Tetzlaff
  fullname: Tetzlaff, W.
  organization: ICORD (International Collaboration On Repair Discoveries), 6270 University Boulevard, University of British Columbia, Vancouver, Canada, V6T 1Z4
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2004; 24
2003; 18
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1997; 9
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1994; 266
1998; 18
1986; 83
2000
1999; 19
1997; 14
2000; 11
2000; 97
1970; 23
2003; 46
1985
1998; 52
1999; 414
1996; 179
1993; 335
1996; 8
1998; 55
1994; 76
1990; 34
2004; 185
2002; 178
2003; 73
1996; 724
1990; 2
1994; 128
1987; 65
2000; 38
1993; 119
2004; 19
2002; 23
2002; 22
2003; 183
1999; 157
1999; 1473
1993; 158
1994; 129
1990; 110
2003; 62
1998; 76
1998; 34
2001; 436
2003; 23
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Snippet The exogenous application of recombinant galectin‐1 has recently been shown to promote the rate of peripheral nerve regeneration. Endogenous neuronal...
The exogenous application of recombinant galectin-1 has recently been shown to promote the rate of peripheral nerve regeneration. Endogenous neuronal...
Abstract The exogenous application of recombinant galectin‐1 has recently been shown to promote the rate of peripheral nerve regeneration. Endogenous neuronal...
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SubjectTerms Animals
Axotomy - methods
Cell Count - methods
Colchicine - pharmacology
Facial Nerve Injuries - metabolism
Facial Nerve Injuries - physiopathology
Functional Laterality - physiology
Galectin 1 - genetics
Galectin 1 - metabolism
GDNF
Gene Expression Regulation - drug effects
Gene Expression Regulation - physiology
Glial Cell Line-Derived Neurotrophic Factor
In Situ Hybridization - methods
L-14
Mice
Mice, Knockout
motoneurons
Motor Neurons - drug effects
Motor Neurons - metabolism
Nerve Crush - methods
Nerve Growth Factors - pharmacology
Nerve Regeneration - physiology
Recovery of Function
regeneration-associated genes
RL14
RNA, Messenger - metabolism
Time Factors
Vibrissae - physiology
Title Galectin-1 in regenerating motoneurons
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https://www.ncbi.nlm.nih.gov/pubmed/15579141
https://search.proquest.com/docview/17319491
https://search.proquest.com/docview/67165962
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