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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

机译:OncostatinM,一种肌肉分泌的肌肌,通过在海马神经元细胞中进行FOS诱导来恢复高葡萄糖诱导的AKT磷酸化损伤

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摘要

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.
机译:OncostatinM是一种肌肉分泌的肌肌,具有各种对神经元功能的影响,然而,潜在的分子机制已定义不足。 在这项研究中,我们表明,OncostatinM增加了Akt和Erk的磷酸化,蛋白质对于神经元细胞存活和增殖至关重要。 此外,OncostatinM通过AKT和ERK增加了C-FOS,一种蛋白质的表达,具有显着涉及神经细胞增殖和存活的蛋白质。 OncostatinM还增加了Akt和Erk的上游的细胞内钙浓度。 用鞘癌素治疗导致高葡萄糖引起的AKT磷酸化损伤的恢复。 因此,OncostatinM可以保护与高葡萄糖条件相关的神经元细胞损伤,显示出作为治疗剂的潜力。 版权所有(c)2019 Wolters Kluwer Health,Inc。保留所有权利。

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