Abstract
Erythropoietin (EPO) has been shown to be a key cytokine in the production of erythrocytes from erythroblasts. Recently, attempts have been made to adopt EPO as a drug target for neuroprotection in selected neurological pathologies. In the current study, a novel EPO-derived peptide which mimics the weak binding site of EPO to its receptor (MK-X) was generated. Experimental results demonstrated that MK-X was able to ameliorate neuronal death due to reactive oxygen species and conditions of oxidative stress similar to EPO. In addition, MK-X induced long-lasting Extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) and Akt activation. Furthermore, treatment with inhibitors of ERK1/2 and Akt abolished the neuroprotective effect of MK-X. Unlike EPO, however, MK-X did not induce cellular proliferation. Collectively, the results of the current study suggested that MK-X may be useful as a novel neuroprotective reagent.
Keywords: Erythropoietin receptor, erythropoietin, neuronal death, peptide, proliferation, reactive oxygen species.
CNS & Neurological Disorders - Drug Targets
Title:Neuroprotective Effects of an Erythropoietin-Derived Peptide in PC1 2 Cells under Oxidative Stress
Volume: 15 Issue: 8
Author(s): Seung-Jun Yoo, Bongki Cho, Chanil Moon, Seong-Woon Yu and Cheil Moon
Affiliation:
Keywords: Erythropoietin receptor, erythropoietin, neuronal death, peptide, proliferation, reactive oxygen species.
Abstract: Erythropoietin (EPO) has been shown to be a key cytokine in the production of erythrocytes from erythroblasts. Recently, attempts have been made to adopt EPO as a drug target for neuroprotection in selected neurological pathologies. In the current study, a novel EPO-derived peptide which mimics the weak binding site of EPO to its receptor (MK-X) was generated. Experimental results demonstrated that MK-X was able to ameliorate neuronal death due to reactive oxygen species and conditions of oxidative stress similar to EPO. In addition, MK-X induced long-lasting Extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) and Akt activation. Furthermore, treatment with inhibitors of ERK1/2 and Akt abolished the neuroprotective effect of MK-X. Unlike EPO, however, MK-X did not induce cellular proliferation. Collectively, the results of the current study suggested that MK-X may be useful as a novel neuroprotective reagent.
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Cite this article as:
Yoo Seung-Jun, Cho Bongki, Moon Chanil, Yu Seong-Woon and Moon Cheil, Neuroprotective Effects of an Erythropoietin-Derived Peptide in PC1 2 Cells under Oxidative Stress, CNS & Neurological Disorders - Drug Targets 2016; 15 (8) . https://dx.doi.org/10.2174/1871527315666160813223329
DOI https://dx.doi.org/10.2174/1871527315666160813223329 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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