Role of the glycoprotein erythropoetin in protection of neurons
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 were thought to be present in the central nervous system according to experiments with antibodies that were subsequently shown to be nonspecific. While erythropoietin alpha is capable of crossing the blood brain barrier via active transport,[1] concentrations in the central nervous system are very low. The possibility that Epo might have effects on neural tissues resulted in experiments to explore whether Epo might be tissue protective. The reported presence of Epo within the spinal fluid of infants and the expression of Epo-R in the spinal cord, suggested a potential role by Epo within the CNS therefore Epo represented a potential therapy to protect photoreceptors damaged from hypoxic pretreatment.[2]
In some animal studies, Epo has been shown to protect nerve cells from hypoxia-induced glutamate toxicity.[2][3] Epo has also been reported to enhance nerve recovery after spinal trauma. Celik and associates investigated motor neuron apoptosis in rabbits with a transient global spinal ischemia model.[4] 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 suggested that RhEpo has both an acute and delayed beneficial action in ischemic spinal cord injury.
In contrast to these results, numerous studies have suggested that Epo had no neuroprotective benefit in animal models and EpoR was not detected in brain tissues using anti-EpoR antibodies that were shown to be sensitive and specific.[citation needed]
^Juul SE, Anderson DK, Li Y, Christensen RD (January 1998). "Erythropoietin and erythropoietin receptor in the developing human central nervous system". Pediatr. Res. 43 (1): 40–9. doi:10.1203/00006450-199804001-00243. PMID 9432111.
^ abGrimm C, Wenzel A, Groszer M, Mayser H, Seeliger M, Samardzija M, Bauer C, Gassmann M, Remé CE (July 2002). "HIF-1-induced erythropoietin in the hypoxic retina protects against light-induced retinal degeneration". Nat. Med. 8 (7): 718–24. doi:10.1038/nm723. PMID 12068288. S2CID 1595426.
^Morishita E, Masuda S, Nagao M, Yasuda Y, Sasaki R (January 1997). "Erythropoietin receptor is expressed in rat hippocampal and cerebral cortical neurons, and erythropoietin prevents in vitro glutamate-induced neuronal death". Neuroscience. 76 (1): 105–16. doi:10.1016/S0306-4522(96)00306-5. PMID 8971763. S2CID 41374229.
^Celik M, Gökmen N, Erbayraktar S, Akhisaroglu M, Konakc S, Ulukus C, Genc S, Genc K, Sagiroglu E, Cerami A, Brines M (February 2002). "Erythropoietin prevents motor neuron apoptosis and neurologic disability in experimental spinal cord ischemic injury". Proc. Natl. Acad. Sci. U.S.A. 99 (4): 2258–63. Bibcode:2002PNAS...99.2258C. doi:10.1073/pnas.042693799. PMC 122352. PMID 11854521.
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