Galectin-1 (Gal-1) has recently been identified as a key molecule that plays important roles in the regulation of neural progenitor cell proliferation in two neurogenic regions: the subventricular zone (SVZ) of the lateral ventricle and the subgranular zone of the hippocampal dentate gyrus. To test the hypothesis that
Gal-1 contributes to adult neurogenesis after focal
ischemia, we studied the temporal profile of endogenous
Gal-1 expression and the effects of human recombinant
Gal-1 on neurogenesis and neurological functions in an experimental focal ischemic model. In the normal brain,
Gal-1 expression was observed only in the SVZ. In the ischemic brain,
Gal-1 expression was markedly upregulated in the SVZ and the area of selective neuronal death around the
infarct in the striatum. The temporal profile of
Gal-1 expression was correlated with that of neural progenitor cell proliferation in the SVZ of the ischemic hemisphere. Double-labeling studies revealed that
Gal-1 was localized predominantly in both reactive astrocytes and SVZ astrocytes. Administration of
Gal-1, which is known to have
carbohydrate-binding ability, into the lateral ventricle increased neurogenesis in the ipsilateral SVZ and improved sensorimotor dysfunction after focal
ischemia. By contrast, blockade of
Gal-1 in the SVZ by the administration of anti-Gal-1
neutralizing antibody strongly inhibited neurogenesis and diminished neurological function. These results suggest that
Gal-1 is one of the principal regulators of adult SVZ neurogenesis through its
carbohydrate-binding ability and provide evidence that
Gal-1 protein has a role in the improvement of sensorimotor function after
stroke.