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Matches in DBpedia 2015-10 for { ?s ?p "Erythropoietin in neuroprotection is the use of the glycoprotein erythropoietin (Epo) for neuroprotection. Epo controls erythropoiesis, or red blood cell production.Erythropoietin and its receptor are both present in the central nervous system with erythropoietin alpha capable of crossing the blood brain barrier via active transport. The presence of Epo within the spinal fluid of infants and the expression of Epo-R in the spinal cord, suggesting a role by Epo within the CNS. Epo and Epo-R is expressed in the mammalian retina, and therefore Epo represents a potential therapy to protect photoreceptors damaged from hypoxic pretreatment.Erythropoietin has been shown to protect nerve cells from hypoxia-induced glutamate toxicity. Acute hypoxia inducement in the adult mouse retina stimulates expression of Epo in addition to other growth factors. Epo response is stimulated by hypoxia and is capable of protecting against apoptosis of erythroid progenitors via a mechanism that is described in the Mechanism of Action section. Epo-R is present in cultured hippocampal and cerebral cortical neurons isolated from rat embryos. Epo was capable of protecting the cultured neurons from glutamate neurotoxicity after only a short exposure. It was concluded that Epo-mediated increase in intracellular calcium concentration is indicative of Epo's neuroprotective role after CNS-related hypoxia or ischemia.Erythropoietin’s role in reducing immune response has been described recently by Michael Brines through his research in administering recombinant human Epo into the blood circulation, which was translocated to the cerebrospinal fluid. RhEpo administer in rats prevented apoptosis of neurons during a cerebral arterial occlusion. It also reduced infarction volume by 75% and decreased post-infarct inflammation.Epo has also been demonstrated to enhance nerve recovery after spinal trauma. Celik and associates investigated motor neuron apoptosis in rabbits with a transient global spinal ischemia model. The functional neurological status of animals given RhEpo was better after recovery from anesthesia, and kept improving over a two-day period. The animals given saline demonstrated a poor functional neurological status and showed no significant improvements. These results showed that RhEpo has both an acute and delayed beneficial action in ischemic spinal cord injury."@en }

• Erythropoietin_in_neuroprotection abstract "Erythropoietin in neuroprotection is the use of the glycoprotein erythropoietin (Epo) for neuroprotection. Epo controls erythropoiesis, or red blood cell production.Erythropoietin and its receptor are both present in the central nervous system with erythropoietin alpha capable of crossing the blood brain barrier via active transport. The presence of Epo within the spinal fluid of infants and the expression of Epo-R in the spinal cord, suggesting a role by Epo within the CNS. Epo and Epo-R is expressed in the mammalian retina, and therefore Epo represents a potential therapy to protect photoreceptors damaged from hypoxic pretreatment.Erythropoietin has been shown to protect nerve cells from hypoxia-induced glutamate toxicity. Acute hypoxia inducement in the adult mouse retina stimulates expression of Epo in addition to other growth factors. Epo response is stimulated by hypoxia and is capable of protecting against apoptosis of erythroid progenitors via a mechanism that is described in the Mechanism of Action section. Epo-R is present in cultured hippocampal and cerebral cortical neurons isolated from rat embryos. Epo was capable of protecting the cultured neurons from glutamate neurotoxicity after only a short exposure. It was concluded that Epo-mediated increase in intracellular calcium concentration is indicative of Epo's neuroprotective role after CNS-related hypoxia or ischemia.Erythropoietin’s role in reducing immune response has been described recently by Michael Brines through his research in administering recombinant human Epo into the blood circulation, which was translocated to the cerebrospinal fluid. RhEpo administer in rats prevented apoptosis of neurons during a cerebral arterial occlusion. It also reduced infarction volume by 75% and decreased post-infarct inflammation.Epo has also been demonstrated to enhance nerve recovery after spinal trauma. Celik and associates investigated motor neuron apoptosis in rabbits with a transient global spinal ischemia model. The functional neurological status of animals given RhEpo was better after recovery from anesthesia, and kept improving over a two-day period. The animals given saline demonstrated a poor functional neurological status and showed no significant improvements. These results showed that RhEpo has both an acute and delayed beneficial action in ischemic spinal cord injury.".