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 mitoc...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Taylor & Francis Group
2021-01-01
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| Series: | Redox Report |
| Subjects: | |
| Online Access: | http://dx.doi.org/10.1080/13510002.2021.1901028 |
| _version_ | 1819177276446605312 |
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| author | Mi Hye Kim Da Yeon Kim Hong Jun Lee Young-Ho Park Jae-Won Huh Dong-Seok Lee |
| author_facet | Mi Hye Kim Da Yeon Kim Hong Jun Lee Young-Ho Park Jae-Won Huh Dong-Seok Lee |
| author_sort | Mi Hye Kim |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-22T21:24:05Z |
| format | Article |
| id | doaj.art-acd1aa8712b748aba6a93a102762b2e6 |
| institution | Directory Open Access Journal |
| issn | 1351-0002 1743-2928 |
| language | English |
| last_indexed | 2024-12-22T21:24:05Z |
| publishDate | 2021-01-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Redox Report |
| spelling | doaj.art-acd1aa8712b748aba6a93a102762b2e62022-12-21T18:12:07ZengTaylor & Francis GroupRedox Report1351-00021743-29282021-01-01261536110.1080/13510002.2021.19010281901028Comparison of the protective effect of cytosolic and mitochondrial Peroxiredoxin 5 against glutamate-induced neuronal cell deathMi Hye Kim0Da Yeon Kim1Hong Jun Lee2Young-Ho Park3Jae-Won Huh4Dong-Seok Lee5Kyungpook National UniversityPusan National University School of MedicineChungbuk National UniversityKorea Research Institute of Bioscience and Biotechnology (KRIBB)Korea Research Institute of Bioscience and Biotechnology (KRIBB)Kyungpook National UniversityObjectives: 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.http://dx.doi.org/10.1080/13510002.2021.1901028cytosolic rosmitochondrial rosapoptosisperoxiredoxin 5glutamateht22hyperhydrogen peroxide |
| spellingShingle | Mi Hye Kim Da Yeon Kim Hong Jun Lee Young-Ho Park Jae-Won Huh Dong-Seok Lee Comparison of the protective effect of cytosolic and mitochondrial Peroxiredoxin 5 against glutamate-induced neuronal cell death Redox Report cytosolic ros mitochondrial ros apoptosis peroxiredoxin 5 glutamate ht22 hyper hydrogen peroxide |
| title | Comparison of the protective effect of cytosolic and mitochondrial Peroxiredoxin 5 against glutamate-induced neuronal cell death |
| title_full | Comparison of the protective effect of cytosolic and mitochondrial Peroxiredoxin 5 against glutamate-induced neuronal cell death |
| title_fullStr | Comparison of the protective effect of cytosolic and mitochondrial Peroxiredoxin 5 against glutamate-induced neuronal cell death |
| title_full_unstemmed | Comparison of the protective effect of cytosolic and mitochondrial Peroxiredoxin 5 against glutamate-induced neuronal cell death |
| title_short | Comparison of the protective effect of cytosolic and mitochondrial Peroxiredoxin 5 against glutamate-induced neuronal cell death |
| title_sort | comparison of the protective effect of cytosolic and mitochondrial peroxiredoxin 5 against glutamate induced neuronal cell death |
| topic | cytosolic ros mitochondrial ros apoptosis peroxiredoxin 5 glutamate ht22 hyper hydrogen peroxide |
| url | http://dx.doi.org/10.1080/13510002.2021.1901028 |
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