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.
Original language | English |
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Pages (from-to) | 765-770 |
Number of pages | 6 |
Journal | Neuroreport |
Volume | 30 |
Issue number | 11 |
DOIs | |
Publication status | Published - 2019 Aug 7 |
Bibliographical note
Publisher Copyright:© 2019 Wolters Kluwer Health, Inc. All rights reserved.
Keywords
- Akt
- ERK
- Oncostatin M
- c-Fos
- high-glucose
ASJC Scopus subject areas
- General Neuroscience