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Arch Orthop Trauma Surg ; 131(6): 829-39, 2011 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-21188398

RESUMEN

INTRODUCTION: Galectin-1 (Gal-1), a carbohydrate-binding protein, is differentially expressed by various normal and pathological tissues and appears to be functionally polyvalent. Recent evidence indicates that Gal-1 is involved in the proliferation of adult neural progenitor cells in neurogenic regions during adulthood. However, localization and functional roles of Gal-1 in the adult spinal cord have not been clarified. METHOD: Here, we investigated the spatio-temporal profile of endogenous Gal-1 expression by in situ hybridization before and after experimental adult spinal cord injury and examined the correlation of Gal-1 with the fate of dividing cells in vivo, using double-labeling methods. Gal-1 mRNA was detectable at a relatively low level in uninjured spinal cord, but was markedly increased in the gray matter and/or white matter and in the ependyma rostral and caudal to the lesion site after injury. RESULTS: Co-localization results revealed that Gal-1 was expressed predominantly by GFAP-positive reactive astrocytes. In addition, intrathecal infusion of recombinant Gal-1 enhanced cell division and reactive astrocytosis in the adult spinal cord. To explore further whether Gal-1 and reactive astrocytes provide a synergistic effect on neurological recovery following SCI, we investigated the differences in behavioral analysis between wild-type (WT) and reactive astrocyte-deficient transgenic mice after injury and found neuroprotective effects of Gal-1 appeared to be specifically mediated through reactive astrocytes. CONCLUSION: These results indicate that Gal-1 exhibits great potential as a novel neuroprotective agent for the treatment of SCI.


Asunto(s)
Astrocitos/fisiología , Galectina 1/fisiología , Traumatismos de la Médula Espinal/fisiopatología , Animales , Astrocitos/efectos de los fármacos , División Celular/fisiología , Galectina 1/análisis , Galectina 1/farmacología , Hibridación in Situ , Locomoción/fisiología , Ratones , Ratones Transgénicos , ARN Mensajero/análisis , Traumatismos de la Médula Espinal/metabolismo , Regulación hacia Arriba
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