The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.
Erythropoietin prevents motor neuron apoptosis and neurologic disability in experimental spinal cord ischemic injury
Open accessAbstract
The cytokine erythropoietin (EPO) possesses potent neuroprotective activity against a variety of potential brain injuries, including transient ischemia and reperfusion. It is currently unknown whether EPO will also ameliorate spinal cord injury. Immunocytochemistry performed using human spinal cord sections showed abundant EPO receptor immunoreactivity of capillaries, especially in white matter, and motor neurons within the ventral horn. We used a transient global spinal ischemia model in rabbits to test whether exogenous EPO can cross the blood–spinal cord barrier and protect these motor neurons. Spinal cord ischemia was produced in rabbits by occlusion of the abdominal aorta for 20 min, followed by saline or recombinant human (rHu)-EPO (350, 800, or 1,000 units/kg of body weight) administered intravenously immediately after the onset of reperfusion. The functional neurological status of animals was better for rHu-EPO-treated animals 1 h after recovery from anesthesia, and improved dramatically over the next 48 h. In contrast, saline-treated animals exhibited a poorer neurological score at 1 h and did not significantly improve. Histopathological examination of the affected spinal cord revealed widespread motor neuron injury associated with positive terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling in control but not in rHu-EPO-treated animals. These observations suggest both an acute as well as a delayed beneficial action of rHu-EPO in ischemic spinal cord injury. Because rHu-EPO is currently used widely with an excellent safety profile, clinical trials evaluating its potential to prevent motor neuron apoptosis and the neurological deficits that occur as a consequence of ischemic injury are warranted.
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Erythropoietin crosses the blood–brain barrier to protect against experimental brain injury
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Self-citationErythropoietin prevents neuronal apoptosis after cerebral ischemia and metabolic stress
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Self-citationIn vivo evidence that erythropoietin protects neurons from ischemic damage
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A Potential Role for Erythropoietin in Focal Permanent Cerebral Ischemia in Mice
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Cited by
Agrawal, M., Saraf, S., Saraf, S., Antimisiaris, S. G., Chougule, M. B., Shoyele, S. A., & Alexander, A. (2018) · Journal of Controlled Release · doi:10.1016/j.jconrel.2018.05.011 · Cited by 630
Emerging biological roles for erythropoietin in the nervous system
Brines, M., & Cerami, A. (2005) · Nature Reviews Neuroscience · doi:10.1038/nrn1687 · Cited by 523
Self-citationErythropoietin as an antiapoptotic, tissue-protective cytokine
Ghezzi, P., & Brines, M. (2004) · Cell Death & Differentiation · doi:10.1038/sj.cdd.4401450 · Cited by 327
Self-citationFrom oxygen to erythropoietin: Relevance of hypoxia for retinal development, health and disease
Caprara, C., & Grimm, C. (2012) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2011.11.003 · Cited by 176
Molecular and cellular immune mediators of neuroprotection
Turrin, N. P., & Rivest, S. (2006) · Molecular Neurobiology · doi:10.1385/mn:34:3:221 · Cited by 85
Metadata
- Authors
- Celik, M., Gökmen, N., Erbayraktar, S., Akhisaroglu, M., Konakç, S., Ulukus, C., Genc, S., Genc, K., Sagiroglu, E., Cerami, A., & Brines, M.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2002-02-19
- Volume
- 99
- Issue
- 4
- Pages
- 2258-2263
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2034987918
- Cited by
- 473
- References
- 24
- FWCI
- 16.76
- Type
- journal article
- Language
- en
- Open access
- green
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- Celik, M., Gökmen, N., Erbayraktar, S., Akhisaroglu, M., Konakç, S., Ulukus, C., Genc, S., Genc, K., Sagiroglu, E., Cerami, A., & Brines, M. (2002). Erythropoietin prevents motor neuron apoptosis and neurologic disability in experimental spinal cord ischemic injury. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.042693799
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