ADAR2-dependent RNA editing of GluR2 is involved in thiamine deficiency-induced alteration of calcium dynamics
文献类型：期刊论文
| 作者 | Lee, Shuchen; Yang, Guang; Yong, Yue; Liu, Ying; Zhao, Liyun; Xu, Jing; Zhang, Xiaomin; Wan, Yanjie; Feng, Chun; Fan, Zhiqin |
| 刊名 | MOLECULAR NEURODEGENERATION
 |
| 出版日期 | 2010 |
| 卷号 | 5期号:1页码:54 |
| 通讯作者 | Luo, J (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Key Lab Nutr & Metab, Shanghai 200031, Peoples R China. |
| 英文摘要 | Background: Thiamine (vitamin B1) deficiency (TD) causes mild impairment of oxidative metabolism and region-selective neuronal loss in the central nervous system (CNS). TD in animals has been used to model aging-associated neurodegeneration in the brain. The mechanisms of TD-induced neuron death are complex, and it is likely multiple mechanisms interplay and contribute to the action of TD. In this study, we demonstrated that TD significantly increased intracellular calcium concentrations [Ca(2+)](i) in cultured cortical neurons. Results: TD drastically potentiated AMPA-triggered calcium influx and inhibited pre-mRNA editing of GluR2, a Ca(2+)-permeable subtype of AMPA receptors. The Ca(2+) permeability of GluR2 is regulated by RNA editing at the Q/R site. Edited GluR2 (R) subunits form Ca(2+)-impermeable channels, whereas unedited GluR2 (Q) channels are permeable to Ca(2+) flow. TD inhibited Q/R editing of GluR2 and increased the ratio of unedited GluR2. The Q/R editing of GluR2 is mediated by adenosine deaminase acting on RNA 2 (ADAR2). TD selectively decreased ADAR2 expression and its self-editing ability without affecting ADAR1 in cultured neurons and in the brain tissue. Overexpression of ADAR2 reduced AMPA-mediated rise of [Ca(2+)](i) and protected cortical neurons against TD-induced cytotoxicity, whereas down-regulation of ADAR2 increased AMPA-elicited Ca(2+) influx and exacerbated TD-induced death of cortical neurons. Conclusions: Our findings suggest that TD-induced neuronal damage may be mediated by the modulation of ADAR2-dependent RNA Editing of GluR2. |
| 类目[WOS] | Neurosciences |
| 研究领域[WOS] | Neurosciences & Neurology |
| 关键词[WOS] | ENDOPLASMIC-RETICULUM STRESS ; CEREBELLAR GRANULE CELLS ; PERMEABLE AMPA RECEPTORS ; OXIDATIVE STRESS ; ADENOSINE-DEAMINASE ; NEURODEGENERATIVE DISEASES ; WERNICKES ENCEPHALOPATHY ; NEUROBLASTOMA-CELLS ; SYNAPTIC PLASTICITY ; CORTICAL-NEURONS |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000285542600001 |
| 公开日期 | 2015-12-24 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/290]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所_糖脂代谢与调控研究组 |
| 推荐引用方式 GB/T 7714 | Lee, Shuchen,Yang, Guang,Yong, Yue,et al. ADAR2-dependent RNA editing of GluR2 is involved in thiamine deficiency-induced alteration of calcium dynamics[J]. MOLECULAR NEURODEGENERATION,2010,5(1):54. |
| APA | Lee, Shuchen.,Yang, Guang.,Yong, Yue.,Liu, Ying.,Zhao, Liyun.,...&Ke, Zun-Ji.(2010).ADAR2-dependent RNA editing of GluR2 is involved in thiamine deficiency-induced alteration of calcium dynamics.MOLECULAR NEURODEGENERATION,5(1),54. |
| MLA | Lee, Shuchen,et al."ADAR2-dependent RNA editing of GluR2 is involved in thiamine deficiency-induced alteration of calcium dynamics".MOLECULAR NEURODEGENERATION 5.1(2010):54. |
入库方式： OAI收割
来源：上海营养与健康研究所
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