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Erythropoietin crosses the blood-brain barrier to protect against experimental brain injury.
TLDR
R-Hu-EPO also ameliorates the extent of concussive brain injury, the immune damage in experimental autoimmune encephalomyelitis, and the toxicity of kainate, and clinical trials evaluating systemically administered r-Hu -EPO as a general neuroprotective treatment are warranted. Expand
Erythropoietin mediates tissue protection through an erythropoietin and common beta-subunit heteroreceptor.
TLDR
The hypothesis that betacR in combination with the EpoR expressed by nonhematopoietic cells constitutes a tissue-protective receptor is hypothesized and supported, as predicted, neither Epo nor CEpo was active in cardiomyocyte or spinal cord injury models performed in the betac R knockout mouse. Expand
Derivatives of Erythropoietin That Are Tissue Protective But Not Erythropoietic
TLDR
CEPO and various nonhematopoietic mutants were cytoprotective in vitro and conferred neuroprotection against stroke, spinal cord compression, diabetic neuropathy, and experimental autoimmune encephalomyelitis at a potency and efficacy comparable to EPO. Expand
Erythropoietin prevents neuronal apoptosis after cerebral ischemia and metabolic stress
TLDR
Data suggest that inhibition of neuronal apoptosis underlies short latency protective effects of EPO after cerebral ischemia and other brain injuries, and the neurotrophic actions suggest there may be longer-latency effects as well. Expand
Erythropoietin Therapy for Acute Stroke Is Both Safe and Beneficial
TLDR
Intravenous high-dose rhEPO is well tolerated in acute ischemic stroke and associated with an improvement in clinical outcome at 1 month, and analysis of covariance controlled for these two variables indicated thatrhEPO treatment was associated with a improvement in follow-up and outcome scales. Expand
Emerging biological roles for erythropoietin in the nervous system
TLDR
New evidence indicates that erythropoietin specifically prevents the destruction of viable tissue surrounding the site of an injury by signalling through a non-haematopoietic receptor. Expand
Erythropoietin‐mediated tissue protection: reducing collateral damage from the primary injury response
TLDR
Effective use of EPO as therapy for tissue injury requires higher doses than for haematopoiesis, potentially triggering serious adverse effects, and the identification of a tissue‐protective receptor isoform has facilitated the engineering of nonhaem atopoietic, tissue-protective EPO derivatives, e.g. carbamyl EPO, that avoid these complications. Expand
Recombinant human erythropoietin protects the myocardium from ischemia-reperfusion injury and promotes beneficial remodeling
TLDR
Observations suggest a potential therapeutic role for recombinant human EPO in the treatment of myocardial ischemia and infarction by preventing apoptosis and attenuating postinfarct deterioration in hemodynamic function, and predict that EPO is likely a tissue-protective cytokine in other organs as well. Expand
Erythropoietin Selectively Attenuates Cytokine Production and Inflammation in Cerebral Ischemia by Targeting Neuronal Apoptosis
TLDR
It is shown that recombinant human EPO markedly reduces astrocyte activation and the recruitment of leukocytes and microglia into an infarction produced by middle cerebral artery occlusion in rats, suggesting that rhEPO attenuates ischemia-induced inflammation by reducing neuronal death rather than by direct effects upon EPO-R–expressing inflammatory cells. Expand
Recombinant human erythropoietin counteracts secondary injury and markedly enhances neurological recovery from experimental spinal cord trauma
TLDR
Observations suggest that rhEPO provides early recovery of function, especially after spinal cord compression, as well as longer-latency neuroprotective, antiinflammatory and antiapoptotic functions. Expand
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