Galectin-1 expression correlates with the regenerative potential of rubrospinal and spinal motoneurons

McGraw, John J.; Oschipok, Loren W.; Liu, J.; Hiebert, Gordon W.; Mak, C.F.W.; Horie, Hidenori; Kadoya, Toshihiko; Steeves, John D.; Ramer, Matt S.; Tetzlaff, Wolfram

doi:10.1016/j.neuroscience.2004.06.075

Cited by 35 publications

(18 citation statements)

References 34 publications

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“…16 Expression of Gal-1 correlates with the regenerative potential of spinal motoneurons after SCI. [17][18][19] Recently, we found that Gal-1 prevents neurodegeneration and promotes neuroprotection in a model of autoimmune neuroinflammation by promoting microglia deactivation. 20 However, in spite of considerable progress, the mechanistic basis of these findings and their therapeutic implications in a setting relevant to human SCI remain unexplored.…”

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confidence: 99%

Glycan-dependent binding of galectin-1 to neuropilin-1 promotes axonal regeneration after spinal cord injury

et al. 2014

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Following spinal cord injury (SCI), semaphorin 3A (Sema3A) prevents axonal regeneration through binding to the neuropilin-1 (NRP-1)/PlexinA4 receptor complex. Here, we show that galectin-1 (Gal-1), an endogenous glycan-binding protein, selectively bound to the NRP-1/PlexinA4 receptor complex in injured neurons through a glycan-dependent mechanism, interrupts the Sema3A pathway and contributes to axonal regeneration and locomotor recovery after SCI. Although both Gal-1 and its monomeric variant contribute to de-activation of microglia, only high concentrations of wild-type Gal-1 (which co-exists in a monomer-dimer equilibrium) bind to the NRP-1/PlexinA4 receptor complex and promote axonal regeneration. Our results show that Gal-1, mainly in its dimeric form, promotes functional recovery of spinal lesions by interfering with inhibitory signals triggered by Sema3A binding to NRP-1/PlexinA4 complex, supporting the use of this lectin for the treatment of SCI patients.

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confidence: 99%

Glycan-dependent binding of galectin-1 to neuropilin-1 promotes axonal regeneration after spinal cord injury

et al. 2014

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“…Previous studies prompt that astrocytic Gal-1 likely act as an endogenous molecule for certain functions following injuries, maybe as a growth-stimulating or survival factor for neurons [26,27] and a chemical mediator of inflammatory response [28]. It also has been confirmed that after 1-day treatment to cerebellar astrocytes with Gal-1, production of BDNF was greatly increased [27].…”

Section: Discussionmentioning

confidence: 87%

Galectin-1 Enhances Astrocytic BDNF Production and Improves Functional Outcome in Rats Following Ischemia

Wang

et al. 2010

Neurochem Res

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Galectin-1, an endogenous mammalian lectin, has been implicated in a variety of CNS disorders. However, its role in cerebral ischemia is still elusive. In the present study, we investigated the effect of recombinant galectin-1 on production of astrocytic brain-derived neurotrophic factor (BDNF) and functional recovery following ischemia. Endogenous galectin-1 was found to be markedly upregulated, paralleled with increased astrocytic BDNF production under ischemic conditions both in vitro and in vivo. Administration of galectin-1 significantly enhanced the expression and secretion of astrocytic BDNF in dose dependent manner. Moreover, rats subjected to photochemical cerebral ischemia showed reduced neuronal apoptosis in ischemic boundary zone and improved functional recovery after brain infusion of galectin-1 (1 μg/days, 7 days). These results suggest that induction of BDNF in astrocytes by galectin-1 may be a promising intervention to attenuate brain damage after stroke.

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“…This response characteristically entails downregulation of certain cellular components, upregulation of others, and even the synthesis of some molecules normally not expressed in adult motoneurons. Thus, while the expression of many proteins involved in neurotransmitter synthesis, packaging, or release -such as choline acetyl-transferase (ChAT), vesicular acetylcholine transporter (VAChT) or the vesicle-associated membrane protein isoform 1 (VAMP-1) -is reduced in axotomized motoneurons, several other cytoskeletal, growth-and survival-associated proteins are strongly upregulated, such as Galectin-1, SCG10, CAP-23, tubulins, kinesin light chains, dynein and certain neurotrophin and cytokine receptors (Leah et al, 1991;Rende et al, 1995;Kobayashi et al, 1996;Fu and Gordon, 1997;Matsuura et al, 1997;Su et al, 1997;Jacobsson et al, 1998;Fernandes et al, 1999;MacLennan et al, 1999;Hammarberg et al, 2000;Tanabe et al, 2000;Mason et al, 2002;Akazawa et al, 2004;Maeda et al, 2004;McGraw et al, 2004;Zujovic et al, 2005). Finally, peripheral lesion of motor axons induces de novo expression of several proteins that are transiently expressed during early development but virtually undetectable in adult motoneurons, such as growth-associated protein 43 (GAP-43), neuronal NO synthase (nNOS), low-affinity p75 nerve growth factor (NGF) receptor or the neuropeptides galanin, somatostatin and vasoactive intestinal peptide (VIP) Palacios et al, 1994;Friedman et al, 1995;Sunico et al, 2005).…”

Section: Traumatic Injury Of a Peripheral Nerve As Model For The Indumentioning

confidence: 99%

Retrograde response in axotomized motoneurons: Nitric oxide as a key player in triggering reversion toward a dedifferentiated phenotype

González-Forero

Moreno‐López

2014

Neuroscience

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The adult brain retains a considerable capacity to functionally reorganize its circuits, which mainly relies on the prevalence of three basic processes that confer plastic potential: synaptic plasticity, plastic changes in intrinsic excitability and, in certain central nervous system (CNS) regions, also neurogenesis. Experimental models of peripheral nerve injury have provided a useful paradigm for studying injury-induced mechanisms of central plasticity. In particular, axotomy of somatic motoneurons triggers a robust retrograde reaction in the CNS, characterized by the expression of plastic changes affecting motoneurons, their synaptic inputs and surrounding glia. Axotomized motoneurons undergo a reprograming of their gene expression and biosynthetic machineries which produce cell components required for axonal regrowth and lead them to resume a functionally dedifferentiated phenotype characterized by the removal of afferent synaptic contacts, atrophy of dendritic arbors and an enhanced somato-dendritic excitability. Although experimental research has provided valuable clues to unravel many basic aspects of this central response, we are still lacking detailed information on the cellular/molecular mechanisms underlying its expression. It becomes clear, however, that the state-switch must be orchestrated by motoneuron-derived signals produced under the direction of the re-activated growth program. Our group has identified the highly reactive gas nitric oxide (NO) as one of these signals, by providing robust evidence for its key role to induce synapse elimination and increases in intrinsic excitability following motor axon damage. We have elucidated operational principles of the NO-triggered downstream transduction pathways mediating each of these changes. Our findings further demonstrate that de novo NO synthesis is not only "necessary" but also "sufficient" to promote the expression of at least some of the features that reflect reversion toward a dedifferentiated state in axotomized adult motoneurons.

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Galectin-1 expression correlates with the regenerative potential of rubrospinal and spinal motoneurons

Cited by 35 publications

References 34 publications

Glycan-dependent binding of galectin-1 to neuropilin-1 promotes axonal regeneration after spinal cord injury

Glycan-dependent binding of galectin-1 to neuropilin-1 promotes axonal regeneration after spinal cord injury

Galectin-1 Enhances Astrocytic BDNF Production and Improves Functional Outcome in Rats Following Ischemia

Retrograde response in axotomized motoneurons: Nitric oxide as a key player in triggering reversion toward a dedifferentiated phenotype

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