Erythropoietin crosses the blood-brain barrier to protect against experimental brain injury
Abstract
Erythropoietin (EPO), recognized for its central role in erythropoiesis, also mediates neuroprotection when the recombinant form (r-Hu-EPO) is directly injected into ischemic rodent brain. We observed abundant expression of the EPO receptor at brain capillaries, which could provide a route for circulating EPO to enter the brain. In confirmation of this hypothesis, systemic administration of r-Hu-EPO before or up to 6 h after focal brain ischemia reduced injury by ≈50–75%. R-Hu-EPO also ameliorates the extent of concussive brain injury, the immune damage in experimental autoimmune encephalomyelitis, and the toxicity of kainate. Given r-Hu-EPO's excellent safety profile, clinical trials evaluating systemically administered r-Hu-EPO as a general neuroprotective treatment are warranted.
Cited By (39)
- Preventive effect of erythropoietin on cardiac dysfunction in doxorubicin-induced cardiomyopathyCirculation · 2006
- Erythropoietin selectively attenuates cytokine production and inflammation in cerebral ischemia by targeting neuronal apoptosisThe Journal of Experimental Medicine · 2003
- Erythropoietin is neuroprotective, improves functional recovery, and reduces neuronal apoptosis and inflammation in a rodent model of experimental closed head injuryThe FASEB Journal · 2005
- Erythropoietin plus insulin‐like growth factor‐I protects against neuronal damage in a murine model of human immunodeficiency virus‐associated neurocognitive disordersAnnals of Neurology · 2010
- Erythropoietin protects neurons against chemical hypoxia and cerebral ischemic injury by up‐regulating Bcl‐xL expressionJournal of Neuroscience Research · 2002
- Erythropoietin protects cardiac myocytes from hypoxia-induced apoptosis through an Akt-dependent pathwayBiochemical and Biophysical Research Communications · 2003
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