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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

Authors
Hyung, William Won SeokLee, Sung GonKim, Keun TaeKim, Hyeon Soo
Issue Date
7-8월-2019
Publisher
LIPPINCOTT WILLIAMS & WILKINS
Keywords
Akt; c-Fos; ERK; high-glucose; Oncostatin M
Citation
NEUROREPORT, v.30, no.11, pp.765 - 770
Indexed
SCIE
SCOPUS
Journal Title
NEUROREPORT
Volume
30
Number
11
Start Page
765
End Page
770
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/63551
DOI
10.1097/WNR.0000000000001271
ISSN
0959-4965
Abstract
Oncostatin 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.
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