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    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; IN-VITRO ; SURVIVAL ; ENDOTHELIAL GROWTH-FACTOR ; Germany ; IN-VIVO ; MODEL ; MODELS ; PATHWAY ; PATHWAYS ; VITRO ; GENERATION ; VOLUME ; DEATH ; DISEASE ; DISEASES ; DRUG ; DIFFERENTIATION ; LIGAND ; MECHANISM ; RAT ; CELL-SURVIVAL ; CELL-DEATH ; LONG-TERM SURVIVAL ; TRANSIENT GLOBAL-ISCHEMIA ; STEM-CELLS ; CENTRAL-NERVOUS-SYSTEM ; COLONY-STIMULATING FACTOR ; STROKE ; signaling ; ADULT ; FOCAL CEREBRAL-ISCHEMIA ; NEURONS ; cell survival ; CEREBRAL-ISCHEMIA ; NEURAL STEM-CELLS ; cell death ; progenitor ; FUNCTIONAL RECOVERY ; MATURE ; RECOVERY ; NEURONAL DIFFERENTIATION ; HIPPOCAMPAL-NEURONS ; FACTOR G-CSF ; INFARCT ; NEWLY GENERATED NEURONS ; RAT DENTATE GYRUS
    Abstract: G-CSF is a potent hematopoietic factor that enhances survival and drives differentiation of myeloid lineage cells, resulting in the generation of neutrophilic granulocytes. Here, we show that G-CSF passes the intact blood-brain barrier and reduces infarct volume in 2 different rat models of acute stroke. G-CSF displays strong antiapoptotic activity in mature neurons and activates multiple cell survival pathways. Both G-CSF and its receptor are widely expressed by neurons in the CNS, and their expression is induced by ischemia, which suggests an autocrine protective signaling mechanism. Surprisingly, the G-CSF receptor was also expressed by adult neural stem cells, and G-CSF induced neuronal differentiation in vitro. G-CSF markedly improved long-term behavioral outcome after cortical ischemia, while stimulating neural progenitor response in vivo, providing a link to functional recovery. Thus, G-CSF is an endogenous ligand in the CNS that has a dual activity beneficial both in counteracting acute neuronal degeneration and contributing to long-term plasticity after cerebral ischemia. We therefore propose G-CSF as a potential new drug for stroke and neurodegenerative diseases
    Type of Publication: Journal article published
    PubMed ID: 16007267
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