Norepinephrine promotes neuronal apoptosis of hippocampal HT22 cells by up-regulating the expression of long non-coding RNA MALAT1
Stress is ever present in our modern, performance-oriented and demanding society, which causes adverse stress reactions of the body and affects health seriously. Chronic stress has been recognized as a significant risk factor leading to cognitive impairment, but the underlying mechanism is far from...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
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Taylor & Francis Group
2023-01-01
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| Series: | Stress |
| Subjects: | |
| Online Access: | http://dx.doi.org/10.1080/10253890.2023.2252905 |
| _version_ | 1797403971933962240 |
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| author | Ying Wang Hui Hu Yuhan Wu Yun Zhao Fang Xie Zhaowei Sun Xue Wang Lingjia Qian |
| author_facet | Ying Wang Hui Hu Yuhan Wu Yun Zhao Fang Xie Zhaowei Sun Xue Wang Lingjia Qian |
| author_sort | Ying Wang |
| collection | DOAJ |
| description | Stress is ever present in our modern, performance-oriented and demanding society, which causes adverse stress reactions of the body and affects health seriously. Chronic stress has been recognized as a significant risk factor leading to cognitive impairment, but the underlying mechanism is far from fully understood. Norepinephrine (NE), a pivotal stress-induced hormone, has been found to induce cell apoptosis. However, the function and the key downstream mediator of NE on the regulation of hippocampal neurons still need further exploration. In this study, we explored the role of NE in neuronal apoptosis and its association with MALAT1. Flow cytometry assay and automated western bot assay were carried out to evaluate the cell apoptosis. The data showed that the rate of apoptosis rate and the levels of apoptotic proteins (cleaved-Caspase3 and cleaved-PARP) were significantly increased in HT22 cells after a high dose of NE treatment, suggesting a facilitative role of NE on hippocampal neuronal apoptosis. Besides, a high level of NE up-regulated the expression of MALAT1 in HT22 cells. Then, a lentivirus expressing MALAT1 shRNA was constructed to investigate the role of MALAT1 in cell apoptosis and the results revealed that MALAT1 depletion decreased the cell apoptosis. Moreover, the knockdown of MALAT1 abolished the discrepancy in apoptosis between NE-treated cells and control cells. In conclusion, a high level of the stress-induced hormone NE promoted apoptosis of hippocampal neurons by elevating the expression of MALAT1. Our findings provide new experimental data supporting the epigenetic mechanisms in the regulation of stress response and may provide a potential therapeutic target for stress-related cognition dysfunction. |
| first_indexed | 2024-03-09T02:47:25Z |
| format | Article |
| id | doaj.art-730f5047c980468a8d5932866e555469 |
| institution | Directory Open Access Journal |
| issn | 1025-3890 1607-8888 |
| language | English |
| last_indexed | 2024-03-09T02:47:25Z |
| publishDate | 2023-01-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Stress |
| spelling | doaj.art-730f5047c980468a8d5932866e5554692023-12-05T16:09:50ZengTaylor & Francis GroupStress1025-38901607-88882023-01-0126110.1080/10253890.2023.22529052252905Norepinephrine promotes neuronal apoptosis of hippocampal HT22 cells by up-regulating the expression of long non-coding RNA MALAT1Ying Wang0Hui Hu1Yuhan Wu2Yun Zhao3Fang Xie4Zhaowei Sun5Xue Wang6Lingjia Qian7Beijing Institute of Basic Medical Sciences, Academy of Military Medical SciencesBeijing Institute of Basic Medical Sciences, Academy of Military Medical SciencesBeijing Institute of Basic Medical Sciences, Academy of Military Medical SciencesBeijing Institute of Basic Medical Sciences, Academy of Military Medical SciencesBeijing Institute of Basic Medical Sciences, Academy of Military Medical SciencesBeijing Institute of Basic Medical Sciences, Academy of Military Medical SciencesBeijing Institute of Basic Medical Sciences, Academy of Military Medical SciencesBeijing Institute of Basic Medical Sciences, Academy of Military Medical SciencesStress is ever present in our modern, performance-oriented and demanding society, which causes adverse stress reactions of the body and affects health seriously. Chronic stress has been recognized as a significant risk factor leading to cognitive impairment, but the underlying mechanism is far from fully understood. Norepinephrine (NE), a pivotal stress-induced hormone, has been found to induce cell apoptosis. However, the function and the key downstream mediator of NE on the regulation of hippocampal neurons still need further exploration. In this study, we explored the role of NE in neuronal apoptosis and its association with MALAT1. Flow cytometry assay and automated western bot assay were carried out to evaluate the cell apoptosis. The data showed that the rate of apoptosis rate and the levels of apoptotic proteins (cleaved-Caspase3 and cleaved-PARP) were significantly increased in HT22 cells after a high dose of NE treatment, suggesting a facilitative role of NE on hippocampal neuronal apoptosis. Besides, a high level of NE up-regulated the expression of MALAT1 in HT22 cells. Then, a lentivirus expressing MALAT1 shRNA was constructed to investigate the role of MALAT1 in cell apoptosis and the results revealed that MALAT1 depletion decreased the cell apoptosis. Moreover, the knockdown of MALAT1 abolished the discrepancy in apoptosis between NE-treated cells and control cells. In conclusion, a high level of the stress-induced hormone NE promoted apoptosis of hippocampal neurons by elevating the expression of MALAT1. Our findings provide new experimental data supporting the epigenetic mechanisms in the regulation of stress response and may provide a potential therapeutic target for stress-related cognition dysfunction.http://dx.doi.org/10.1080/10253890.2023.2252905nemalat1apoptosisht22lncrnastress |
| spellingShingle | Ying Wang Hui Hu Yuhan Wu Yun Zhao Fang Xie Zhaowei Sun Xue Wang Lingjia Qian Norepinephrine promotes neuronal apoptosis of hippocampal HT22 cells by up-regulating the expression of long non-coding RNA MALAT1 Stress ne malat1 apoptosis ht22 lncrna stress |
| title | Norepinephrine promotes neuronal apoptosis of hippocampal HT22 cells by up-regulating the expression of long non-coding RNA MALAT1 |
| title_full | Norepinephrine promotes neuronal apoptosis of hippocampal HT22 cells by up-regulating the expression of long non-coding RNA MALAT1 |
| title_fullStr | Norepinephrine promotes neuronal apoptosis of hippocampal HT22 cells by up-regulating the expression of long non-coding RNA MALAT1 |
| title_full_unstemmed | Norepinephrine promotes neuronal apoptosis of hippocampal HT22 cells by up-regulating the expression of long non-coding RNA MALAT1 |
| title_short | Norepinephrine promotes neuronal apoptosis of hippocampal HT22 cells by up-regulating the expression of long non-coding RNA MALAT1 |
| title_sort | norepinephrine promotes neuronal apoptosis of hippocampal ht22 cells by up regulating the expression of long non coding rna malat1 |
| topic | ne malat1 apoptosis ht22 lncrna stress |
| url | http://dx.doi.org/10.1080/10253890.2023.2252905 |
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