A carbohydrate-binding protein, Galectin-1, promotes proliferation of adult neural stem cells

Sakaguchi, Masanori; Shingo, Tetsuro; Shimazaki, Takuya; Okano, Hirotaka James; Shiwa, Mieko; Ishibashi, Satoru; Oguro, Hideyuki; Ninomiya, Mikiko; Kadoya, Toshihiko; Horie, Hidenori; Shibuya, Akira; Mizusawa, Hidehiro; Poirier, Françoise; Nakauchi, Hiromitsu; Sawamoto, Kazunobu; Okano, Hideyuki

doi:10.1073/pnas.0508793103

Cited by 144 publications

(166 citation statements)

References 53 publications

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“…3E). As also Lgals1 is significantly upregulated in reactive astrocytes and both have been implicated in regulating adult NSCs (Beckervordersandforth et al, 2010; Di Lella et al, 2011; Kajitani et al, 2009; Sakaguchi et al, 2006; Yan et al, 2009), this prompted us to focus on the role of Lgals1 and Lgals3 in the injured cerebral cortex.…”

Section: Resultsmentioning

confidence: 99%

Astrocyte reactivity after brain injury—: The role of galectins 1 and 3

Sirko

Irmler

Gascón

et al. 2015

Glia

116

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Astrocytes react to brain injury in a heterogeneous manner with only a subset resuming proliferation and acquiring stem cell properties in vitro. In order to identify novel regulators of this subset, we performed genomewide expression analysis of reactive astrocytes isolated 5 days after stab wound injury from the gray matter of adult mouse cerebral cortex. The expression pattern was compared with astrocytes from intact cortex and adult neural stem cells (NSCs) isolated from the subependymal zone (SEZ). These comparisons revealed a set of genes expressed at higher levels in both endogenous NSCs and reactive astrocytes, including two lectins—Galectins 1 and 3. These results and the pattern of Galectin expression in the lesioned brain led us to examine the functional significance of these lectins in brains of mice lacking Galectins 1 and 3. Following stab wound injury, astrocyte reactivity including glial fibrillary acidic protein expression, proliferation and neurosphere‐forming capacity were found significantly reduced in mutant animals. This phenotype could be recapitulated in vitro and was fully rescued by addition of Galectin 3, but not of Galectin 1. Thus, Galectins 1 and 3 play key roles in regulating the proliferative and NSC potential of a subset of reactive astrocytes. GLIA 2015;63:2340–2361

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Section: Resultsmentioning

confidence: 99%

Astrocyte reactivity after brain injury—: The role of galectins 1 and 3

Sirko

Irmler

Gascón

et al. 2015

Glia

116

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“…Proliferating cells in the DG were labeled by short-or long-term administration of BrdU as previously described (Sakaguchi et al, 2006). Briefly, for long-term labeling, mice were administered 1 mg/ml of BrdU via the drinking water for 2 weeks and killed 4 weeks after the last day of administration.…”

Section: Methodsmentioning

confidence: 99%

Sox21 Promotes Hippocampal Adult Neurogenesis via the Transcriptional Repression of theHes5Gene

et al. 2012

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“…This lectin exists in a monomer-dimer equilibrium depending on its relative concentration and biochemical features of different tissues. 13 Within the CNS, Gal-1 controls proliferation of adult neural progenitor cells, 14,15 regulates neurogenesis and promotes functional recovery after stroke. 16 Expression of Gal-1 correlates with the regenerative potential of spinal motoneurons after SCI.…”

mentioning

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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A carbohydrate-binding protein, Galectin-1, promotes proliferation of adult neural stem cells

Cited by 144 publications

References 53 publications

Astrocyte reactivity after brain injury—: The role of galectins 1 and 3

Astrocyte reactivity after brain injury—: The role of galectins 1 and 3

Sox21 Promotes Hippocampal Adult Neurogenesis via the Transcriptional Repression of theHes5Gene

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

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