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Oncostatin M, a muscle-secreted myokine, recovers high-glucose-induced impairment of Akt phosphorylation by Fos induction in hippocampal neuron cells

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dc.contributor.authorHyung, William Won Seok-
dc.contributor.authorLee, Sung Gon-
dc.contributor.authorKim, Keun Tae-
dc.contributor.authorKim, Hyeon Soo-
dc.date.accessioned2021-09-01T09:38:56Z-
dc.date.available2021-09-01T09:38:56Z-
dc.date.created2021-06-18-
dc.date.issued2019-08-07-
dc.identifier.issn0959-4965-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/63551-
dc.description.abstractOncostatin M is a muscle-secreted myokine that has various effects on neuronal function, however, the underlying molecular mechanism has been poorly defined. In this study, we showed that Oncostatin M increased the phosphorylation of Akt and ERK, proteins crucial for neuron cell survival and proliferation. Furthermore, Oncostatin M increased the expression of c-Fos, a protein with significant involvement in neuronal cell proliferation and survival, through both Akt and ERK. Oncostatin M also increased intracellular calcium concentrations that act upstream of Akt and ERK. Treatment with Oncostatin M led to the recovery of high-glucose-induced impairment of Akt phosphorylation. Thus, Oncostatin M can protect neuronal cell damage related to high-glucose conditions, showing potential as a therapeutic agent. Copyright (C) 2019 Wolters Kluwer Health, Inc. All rights reserved.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherLIPPINCOTT WILLIAMS & WILKINS-
dc.subjectALZHEIMERS-DISEASE-
dc.subjectINSULIN-RESISTANCE-
dc.subjectEXERCISE-
dc.subjectINTERLEUKIN-6-
dc.subjectPATHOGENESIS-
dc.titleOncostatin M, a muscle-secreted myokine, recovers high-glucose-induced impairment of Akt phosphorylation by Fos induction in hippocampal neuron cells-
dc.typeArticle-
dc.contributor.affiliatedAuthorKim, Hyeon Soo-
dc.identifier.doi10.1097/WNR.0000000000001271-
dc.identifier.scopusid2-s2.0-85069264476-
dc.identifier.wosid000480684000003-
dc.identifier.bibliographicCitationNEUROREPORT, v.30, no.11, pp.765 - 770-
dc.relation.isPartOfNEUROREPORT-
dc.citation.titleNEUROREPORT-
dc.citation.volume30-
dc.citation.number11-
dc.citation.startPage765-
dc.citation.endPage770-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.subject.keywordPlusALZHEIMERS-DISEASE-
dc.subject.keywordPlusINSULIN-RESISTANCE-
dc.subject.keywordPlusEXERCISE-
dc.subject.keywordPlusINTERLEUKIN-6-
dc.subject.keywordPlusPATHOGENESIS-
dc.subject.keywordAuthorAkt-
dc.subject.keywordAuthorc-Fos-
dc.subject.keywordAuthorERK-
dc.subject.keywordAuthorhigh-glucose-
dc.subject.keywordAuthorOncostatin M-
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