Journal of Neurochemistry · 2010 · 41 citations · 39 references
Cell DeathFocal Cerebral IschemiaActivated AstrocytesSocial SciencesOxidative StressNeuroinflammationInflammationDisease PhysiologyCerebral Vascular RegulationNeuroregenerationBrain InjuryNeurologyNeuroimmunologyMolecular SignalingExcessive AstrogliosisBrain IschemiaBrain-immune InteractionVascular BiologyNeuroprotectionCerebral Blood FlowReperfusion InjuryPharmacologyCell BiologyNeurodegenerative DiseasesNeuroscienceMedicine
Astrogliosis occurs after brain ischemia, and excessive astrogliosis can devastate the neuronal recovery. Previous reports show that galectin-1 (Gal-1) regulates proliferation of several cell types and plays an important role after nervous system injuries. Here, we found that expression of Gal-1 was remarkably up-regulated in activated astrocytes around ischemic infarct. Furthermore, under ischemic conditions either in vitro or in vivo, Gal-1 was found to inhibit the proliferation of astrocytes in a dose-dependent manner, attenuate astrogliosis and down-regulate the astrogliosis associated expression of nitric oxide synthase and interleukin-1β after the ischemia. All these changes were blocked by lactose, suggesting a lectin dependent manner of Gal-1's function. Moreover, 7-day Gal-1 treatment reduced apoptosis of neurons, decreased brain infarction volume and improved neurological function induced by the ischemia. Together, these findings indicate that through reducing astrogliosis related damages, Gal-1 is a potential therapeutical target for attenuating neuronal damage and promoting recovery of brain ischemia.
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Simone Di Giovanni, Vilen Movsesyan, Farid Ahmed et al. · Proceedings of the National Academy of Sciences · 2005 · 376 citations · Full text
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