Dual cell protective mechanisms activated by differing levels of oxidative stress in HT22 murine hippocampal cells
Dual cell protective mechanisms activated by differing levels of oxidative stress in HT22 murine hippocampal cells
复制标题
HT22小鼠海马细胞不同氧化应激水平激活的双重细胞保护机制
DOI：
10.1080/09168451.2014.936343
复制
发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Nedachi T
中科院分区：
文献类型：
--
作者：
Sato K;Yamanaka Y;Ishii M;Ishibashi K;Ogura Y;Ohtani-Kaneko R;Nishihara M;Nedachi T
氧化应激被认为是神经退行性疾病的致病机制之一。然而，最近的证据表明，调节细胞命运的氧化应激反应似乎是依赖于应激水平。在这项研究中，使用HT 22细胞，我们试图了解氧化应激水平的改变如何影响神经元细胞的命运。HT 22细胞活力降低暴露于高水平的氧化应激，而低水平的氧化应激促进细胞存活。低水平的氧化应激诱导的Erk 1/2活化在这种细胞保护作用中发挥了作用。有趣的是，亚毒性水平的H2 O2诱导的生长因子前颗粒蛋白（PGRN）的表达和外源性PGRN预处理以Erk 1/2依赖的方式减弱了高浓度H2 O2诱导的HT 22细胞死亡。总之，我们的研究表明，两种不同的细胞保护机制被HT 22细胞中不同水平的氧化应激激活。
Oxidative stress is recognized as one of the pathogenic mechanisms involved in neurodegenerative disease. However, recent evidence has suggested that regulation of cellular fate in response to oxidative stress appears to be dependent on the stress levels. In this study, using HT22 cells, we attempted to understand how an alteration in the oxidative stress levels would influence neuronal cell fate. HT22 cell viability was reduced with exposure to high levels of oxidative stress, whereas, low levels of oxidative stress promoted cell survival. Erk1/2 activation induced by a low level of oxidative stress played a role in this cell protective effect. Intriguingly, subtoxic level of H2O2induced expression of a growth factor, progranulin (PGRN), and exogenous PGRN pretreatment attenuated HT22 cell death induced by high concentrations of H2O2in Erk1/2-dependent manner. Together, our study indicates that two different cell protection mechanisms are activated by differing levels of oxidative stress in HT22 cells.