胞质过氧化氧还蛋白5和线粒体过氧化氧还蛋白5对谷氨酸诱导的神经元细胞死亡的保护作用比较。

IF 5.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Mi Hye Kim, Da Yeon Kim, Hong Jun Lee, Young-Ho Park, Jae-Won Huh, Dong-Seok Lee
{"title":"胞质过氧化氧还蛋白5和线粒体过氧化氧还蛋白5对谷氨酸诱导的神经元细胞死亡的保护作用比较。","authors":"Mi Hye Kim,&nbsp;Da Yeon Kim,&nbsp;Hong Jun Lee,&nbsp;Young-Ho Park,&nbsp;Jae-Won Huh,&nbsp;Dong-Seok Lee","doi":"10.1080/13510002.2021.1901028","DOIUrl":null,"url":null,"abstract":"<p><p><b>Objectives</b>: Although glutamate is an essential factor in the neuronal system, excess glutamate can produce excitotoxicity. We previously reported that Peroxiredoxin 5 (Prx5) protects neuronal cells from glutamate toxicity via its antioxidant effects. However, it is unclear whether cytosolic or mitochondrial Prx5 provides greater neuroprotection. Here, we investigated differences in the neuroprotective effects of cytosolic and mitochondrial Prx5.<b>Methods</b>: We analyzed patterns of cytosolic and mitochondrial H<sub>2</sub>O<sub>2</sub> generation in glutamate toxicity using HyPer protein. And then, we confirmed the change of intracellular ROS level and apoptosis with respective methods. The mitochondrial dynamics was assessed with confocal microscope imaging and western blotting.<b>Results</b>: We found that the level of mitochondrial H<sub>2</sub>O<sub>2</sub> greatly increased compared to cytosolic H<sub>2</sub>O<sub>2</sub> and it affected cytosolic H<sub>2</sub>O<sub>2</sub> generation after glutamate treatment. In addition, we confirmed that mitochondrial Prx5 provides more effective neuroprotection than cytosolic Prx5.<b>Discussion</b>: Overall, our study reveals the mechanisms of cytosolic and mitochondrial ROS in glutamate toxicity. Our findings suggest that mitochondrial ROS and Prx5 are attractive therapeutic targets and that controlling these factors be useful for the prevention of neurodegenerative diseases.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":null,"pages":null},"PeriodicalIF":5.2000,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/13510002.2021.1901028","citationCount":"2","resultStr":"{\"title\":\"Comparison of the protective effect of cytosolic and mitochondrial Peroxiredoxin 5 against glutamate-induced neuronal cell death.\",\"authors\":\"Mi Hye Kim,&nbsp;Da Yeon Kim,&nbsp;Hong Jun Lee,&nbsp;Young-Ho Park,&nbsp;Jae-Won Huh,&nbsp;Dong-Seok Lee\",\"doi\":\"10.1080/13510002.2021.1901028\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p><b>Objectives</b>: Although glutamate is an essential factor in the neuronal system, excess glutamate can produce excitotoxicity. We previously reported that Peroxiredoxin 5 (Prx5) protects neuronal cells from glutamate toxicity via its antioxidant effects. However, it is unclear whether cytosolic or mitochondrial Prx5 provides greater neuroprotection. Here, we investigated differences in the neuroprotective effects of cytosolic and mitochondrial Prx5.<b>Methods</b>: We analyzed patterns of cytosolic and mitochondrial H<sub>2</sub>O<sub>2</sub> generation in glutamate toxicity using HyPer protein. And then, we confirmed the change of intracellular ROS level and apoptosis with respective methods. The mitochondrial dynamics was assessed with confocal microscope imaging and western blotting.<b>Results</b>: We found that the level of mitochondrial H<sub>2</sub>O<sub>2</sub> greatly increased compared to cytosolic H<sub>2</sub>O<sub>2</sub> and it affected cytosolic H<sub>2</sub>O<sub>2</sub> generation after glutamate treatment. In addition, we confirmed that mitochondrial Prx5 provides more effective neuroprotection than cytosolic Prx5.<b>Discussion</b>: Overall, our study reveals the mechanisms of cytosolic and mitochondrial ROS in glutamate toxicity. Our findings suggest that mitochondrial ROS and Prx5 are attractive therapeutic targets and that controlling these factors be useful for the prevention of neurodegenerative diseases.</p>\",\"PeriodicalId\":21096,\"journal\":{\"name\":\"Redox Report\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":5.2000,\"publicationDate\":\"2021-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1080/13510002.2021.1901028\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Redox Report\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1080/13510002.2021.1901028\",\"RegionNum\":2,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Redox Report","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1080/13510002.2021.1901028","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 2

摘要

目的:虽然谷氨酸是神经系统的重要因子,但过量的谷氨酸会产生兴奋性毒性。我们之前报道过过氧化物还蛋白5 (Prx5)通过其抗氧化作用保护神经细胞免受谷氨酸的毒性。然而,尚不清楚是细胞质Prx5还是线粒体Prx5提供了更大的神经保护作用。在这里,我们研究了胞质和线粒体Prx5在神经保护作用方面的差异。方法:利用超蛋白分析谷氨酸中毒时细胞质和线粒体产生H2O2的模式。然后分别用不同的方法证实细胞内ROS水平和凋亡的变化。用共聚焦显微镜成像和免疫印迹法观察线粒体动力学。结果:我们发现谷氨酸处理后线粒体H2O2水平较胞质H2O2显著升高,影响胞质H2O2的生成。此外,我们证实线粒体Prx5比细胞质Prx5提供更有效的神经保护。讨论:总的来说,我们的研究揭示了细胞质和线粒体ROS在谷氨酸毒性中的机制。我们的研究结果表明,线粒体ROS和Prx5是有吸引力的治疗靶点,控制这些因素有助于预防神经退行性疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Comparison of the protective effect of cytosolic and mitochondrial Peroxiredoxin 5 against glutamate-induced neuronal cell death.

Comparison of the protective effect of cytosolic and mitochondrial Peroxiredoxin 5 against glutamate-induced neuronal cell death.

Comparison of the protective effect of cytosolic and mitochondrial Peroxiredoxin 5 against glutamate-induced neuronal cell death.

Comparison of the protective effect of cytosolic and mitochondrial Peroxiredoxin 5 against glutamate-induced neuronal cell death.

Objectives: Although glutamate is an essential factor in the neuronal system, excess glutamate can produce excitotoxicity. We previously reported that Peroxiredoxin 5 (Prx5) protects neuronal cells from glutamate toxicity via its antioxidant effects. However, it is unclear whether cytosolic or mitochondrial Prx5 provides greater neuroprotection. Here, we investigated differences in the neuroprotective effects of cytosolic and mitochondrial Prx5.Methods: We analyzed patterns of cytosolic and mitochondrial H2O2 generation in glutamate toxicity using HyPer protein. And then, we confirmed the change of intracellular ROS level and apoptosis with respective methods. The mitochondrial dynamics was assessed with confocal microscope imaging and western blotting.Results: We found that the level of mitochondrial H2O2 greatly increased compared to cytosolic H2O2 and it affected cytosolic H2O2 generation after glutamate treatment. In addition, we confirmed that mitochondrial Prx5 provides more effective neuroprotection than cytosolic Prx5.Discussion: Overall, our study reveals the mechanisms of cytosolic and mitochondrial ROS in glutamate toxicity. Our findings suggest that mitochondrial ROS and Prx5 are attractive therapeutic targets and that controlling these factors be useful for the prevention of neurodegenerative diseases.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Redox Report
Redox Report 生物-生化与分子生物学
CiteScore
6.10
自引率
0.00%
发文量
28
审稿时长
>12 weeks
期刊介绍: Redox Report is a multidisciplinary peer-reviewed open access journal focusing on the role of free radicals, oxidative stress, activated oxygen, perioxidative and redox processes, primarily in the human environment and human pathology. Relevant papers on the animal and plant environment, biology and pathology will also be included. While emphasis is placed upon methodological and intellectual advances underpinned by new data, the journal offers scope for review, hypotheses, critiques and other forms of discussion.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信