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.
