Escitalopram Ameliorates Forskolin-Induced Tau Hyperphosphorylation in HEK239/tau441 Cells
文献类型：期刊论文
| 作者 | Ren QG[*]1,2; Wang YJ1; Gong WG1; Zhou QD2; Xu L3,4; Zhang ZJ[*]1 |
| 刊名 | JOURNAL OF MOLECULAR NEUROSCIENCE
 |
| 出版日期 | 2015 |
| 卷号 | 56期号:2页码:500-508 |
| 关键词 | Tau Escitalopram GSK-3 beta SSRI |
| 通讯作者 | rqg1976@tom.com ; zhijunzhang@seu.edu.cn |
| 合作状况 | 其它 |
| 英文摘要 | To investigate the effect of escitalopram (a widely used and highly efficacious antidepressant from the SSRI class) on tau hyperphosphorylation, HEK293/tau441 cells were pretreated with 4 mu M of forskolin for 2 h. Then we treated the cells with different doses of escitalopram (0, 5, 10, 20, 40, 80 mu M) for 22 h. We measured the phosphorylation level of tau by Western blotting. It was shown that escitalopram could protect tau from hyperphosphorylation induced by pharmacological activation of protein kinase A (PKA) at a dose of 20, 40, and 80 mu M in vitro. Interestingly, the same dose of escitalopram could also increase the level of serine-9-phosphorylated GSK-3 beta (inactive form) and the phosphorylation level of Akt at Ser473 (active form) with no significant change in the level of total GSK-3 beta and Akt. Unexpectedly, 5-hydroxytryptamine 1A receptor (5-HT1A) agonist 8-OH-DPAT did not decrease forskolin-induced tau hyperphosphorylation. Our results suggest that escitalopram can ameliorate forskolin-induced tau hyperphosphorylation, which is not through the typical 5-HT1A pathway, and Akt/GSK-3 beta signaling pathway is involved. These findings may support an effective role of antidepressants in the prevention of dementia associated with depression in patients. |
| 收录类别 | SCI |
| 资助信息 | This work was supported in part by grantsf rom the National Natural Science Foundation of China (30900447 and 91232707), grants from the National Basic Research Program of China (2013CB835103), Strategic Priority Research Program of Chinese Acad- emy of Science (XDB02020002), Bthe Fundamental Research Funds for the Central Universities^, and Bthe ordinary university graduate research and innovation program in Jiangsu Province^ (KYLX_0200). |
| 语种 | 英语 |
| 源URL | [http://159.226.149.26:8080/handle/152453/9186]  |
| 专题 | 昆明动物研究所_学习记忆的分子神经机制 昆明动物研究所_动物模型与人类重大疾病机理重点实验室 |
| 作者单位 | 1.Department of Neuropsychiatry, Affiliated ZhongDa Hospital, School of Medicine, Southeast University, Nanjing, China 2.Department of Neurology, Wu Xi Branch of Affiliated ZhongDa Hospital, School of Medicine, Southeast University, Wuxi, China 3.Key Laboratory of Animal Models and Human Disease Mechanisms, Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Kunming, Yunnan, China 4.Graduate School of Chinese Academy of Sciences, Beijing, China |
| 推荐引用方式 GB/T 7714 | Ren QG[*],Wang YJ,Gong WG,et al. Escitalopram Ameliorates Forskolin-Induced Tau Hyperphosphorylation in HEK239/tau441 Cells[J]. JOURNAL OF MOLECULAR NEUROSCIENCE,2015,56(2):500-508. |
| APA | Ren QG[*],Wang YJ,Gong WG,Zhou QD,Xu L,&Zhang ZJ[*].(2015).Escitalopram Ameliorates Forskolin-Induced Tau Hyperphosphorylation in HEK239/tau441 Cells.JOURNAL OF MOLECULAR NEUROSCIENCE,56(2),500-508. |
| MLA | Ren QG[*],et al."Escitalopram Ameliorates Forskolin-Induced Tau Hyperphosphorylation in HEK239/tau441 Cells".JOURNAL OF MOLECULAR NEUROSCIENCE 56.2(2015):500-508. |
入库方式： OAI收割
来源：昆明动物研究所
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