SIRT3 deacetylated and increased citrate synthase activity in PD model
SIRT3 deacetylated and increased citrate synthase activity in PD model
复制标题
SIRT3 在 PD 模型中去乙酰化并增加柠檬酸合酶活性
DOI：
10.1016/j.bbrc.2017.01.163
复制
发表时间：
2017-03-18
影响因子：
3.1
通讯作者：
Wu, Yun-Cheng
中科院分区：
文献类型：
--
作者：
Cui, Xin-Xin;Li, Xuan;Wu, Yun-Cheng
已发现SIRT3在许多神经系统疾病中具有神经保护作用，但其详细机制仅部分了解。本研究采用MPP+处理SH-SY5Y细胞作为PD的细胞模型，检测SIRT3的作用及其可能参与的机制。我们重点研究了SIRT3与线粒体关键酶柠檬酸合成酶（CS）和异柠檬酸脱氢酶2 （IDH2）的变化及其关系。我们发现MPP+降低了SIRT3的表达。结果表明，在MPP+处理细胞中，CS和IDH2的酶活性显著降低，而CS和IDH2的蛋白乙酰化程度升高。但过表达的sirt3至少部分逆转了CS活性的下降和CS蛋白乙酰化的增加。IDH2没有出现相同的变化。研究表明SIRT3脱乙酰化并激活CS活性。因此，我们得出结论，SIRT3通过去乙酰化和增加线粒体酶活性表现出神经保护作用。(C) 2017爱思唯尔公司版权所有。
SIRT3 have been found to be neuroprotective in many neurological diseases, but its detail mechanism is only partially understood. In this study, MPP+ was used to treat SH-SY5Y cells as the cellular model of PD to test the role of SIRT3 and the mechanism may be involved in. We focused on the changes and relationship between SIRT3 and the key mitochondrial enzymes citrate synthase (CS) and isocitrate dehydrogenase 2 (IDH2). We found MPP+ decreased SIRT3 expression. And our results showed that the enzymatic activities of CS and IDH2 were significantly reduced in MPP+ treatment cells, while protein acetylation of CS and IDH2 increased. However overexpressed-SIRT3 partially reversed at least, the decline of CS activity and the increase of CS protein acetylation. IDH2 did not showed the same changes. The study suggested that SIRT3 deacetylated and activated CS activity. Hence, we conclude that SIRT3 exhibits neuroprotection via deacetylating and increasing mitochondrial enzyme activities. (C) 2017 Elsevier Inc. All rights reserved.