SPARC Knockdown Reduces Glutamate-Induced HT22 Hippocampal Nerve Cell Damage by Regulating Autophagy
Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein involved in the extracellular matrix and interactions between cells during neural development of the central nervous system (CNS). Oxidative glutamate toxicity is involved in CNS diseases, including epilepsy, Alzheimer’s...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2021-01-01
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| Series: | Frontiers in Neuroscience |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fnins.2020.581441/full |
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doaj-1ac51bd9a1af44068e0dc893e3e4847e |
|---|---|
| record_format |
Article |
| collection |
DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
Shuang Chen Shuang Chen Qin Zou Qiang Guo Yongmin Chen Yongmin Chen Xi Kuang Xi Kuang Yukang Zhang Yukang Zhang Yan Liu Yan Liu Wengang Wu Wengang Wu Ge Li Ge Li Linzhi Tu Linzhi Tu Jingyi Tong Jingyi Tong Songrong Li Songrong Li Lin Ma Lin Ma Qifu Li Qifu Li |
| spellingShingle |
Shuang Chen Shuang Chen Qin Zou Qiang Guo Yongmin Chen Yongmin Chen Xi Kuang Xi Kuang Yukang Zhang Yukang Zhang Yan Liu Yan Liu Wengang Wu Wengang Wu Ge Li Ge Li Linzhi Tu Linzhi Tu Jingyi Tong Jingyi Tong Songrong Li Songrong Li Lin Ma Lin Ma Qifu Li Qifu Li SPARC Knockdown Reduces Glutamate-Induced HT22 Hippocampal Nerve Cell Damage by Regulating Autophagy Frontiers in Neuroscience SPARC autophagy glutamate HT22 epilepsy neurological diseases |
| author_facet |
Shuang Chen Shuang Chen Qin Zou Qiang Guo Yongmin Chen Yongmin Chen Xi Kuang Xi Kuang Yukang Zhang Yukang Zhang Yan Liu Yan Liu Wengang Wu Wengang Wu Ge Li Ge Li Linzhi Tu Linzhi Tu Jingyi Tong Jingyi Tong Songrong Li Songrong Li Lin Ma Lin Ma Qifu Li Qifu Li |
| author_sort |
Shuang Chen |
| title |
SPARC Knockdown Reduces Glutamate-Induced HT22 Hippocampal Nerve Cell Damage by Regulating Autophagy |
| title_short |
SPARC Knockdown Reduces Glutamate-Induced HT22 Hippocampal Nerve Cell Damage by Regulating Autophagy |
| title_full |
SPARC Knockdown Reduces Glutamate-Induced HT22 Hippocampal Nerve Cell Damage by Regulating Autophagy |
| title_fullStr |
SPARC Knockdown Reduces Glutamate-Induced HT22 Hippocampal Nerve Cell Damage by Regulating Autophagy |
| title_full_unstemmed |
SPARC Knockdown Reduces Glutamate-Induced HT22 Hippocampal Nerve Cell Damage by Regulating Autophagy |
| title_sort |
sparc knockdown reduces glutamate-induced ht22 hippocampal nerve cell damage by regulating autophagy |
| publisher |
Frontiers Media S.A. |
| series |
Frontiers in Neuroscience |
| issn |
1662-453X |
| publishDate |
2021-01-01 |
| description |
Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein involved in the extracellular matrix and interactions between cells during neural development of the central nervous system (CNS). Oxidative glutamate toxicity is involved in CNS diseases, including epilepsy, Alzheimer’s disease, and ischemic stroke. However, the molecular mechanism of nerve injury is not fully understood in CNS diseases. Herein, the glutamate-induced nerve damage model was used to explore the molecular mechanisms affecting nerve damage. The levels of SPARC and autophagy were increased in glutamate-induced HT22 hippocampal nerve injury. In summary, the current study confirmed that SPARC regulates autophagy in HT22 hippocampal nerve cells, and its knockdown reduces the glutamate-induced HT22 hippocampal nerve injury by inhibiting autophagy. These findings suggested that SPARC plays a crucial role in nerve injury of CNS diseases. |
| topic |
SPARC autophagy glutamate HT22 epilepsy neurological diseases |
| url |
https://www.frontiersin.org/articles/10.3389/fnins.2020.581441/full |
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doaj-1ac51bd9a1af44068e0dc893e3e4847e2021-01-26T05:09:21ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2021-01-011410.3389/fnins.2020.581441581441SPARC Knockdown Reduces Glutamate-Induced HT22 Hippocampal Nerve Cell Damage by Regulating AutophagyShuang Chen0Shuang Chen1Qin Zou2Qiang Guo3Yongmin Chen4Yongmin Chen5Xi Kuang6Xi Kuang7Yukang Zhang8Yukang Zhang9Yan Liu10Yan Liu11Wengang Wu12Wengang Wu13Ge Li14Ge Li15Linzhi Tu16Linzhi Tu17Jingyi Tong18Jingyi Tong19Songrong Li20Songrong Li21Lin Ma22Lin Ma23Qifu Li24Qifu Li25Department of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, ChinaKey Laboratory of Brain Science Research & Transformation in Tropical Environment of Hainan Province, Hainan Medical University, Haikou, ChinaDepartment of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, ChinaEpilepsy Center, Guangdong Sanjiu Brain Hospital, Guangzhou, ChinaDepartment of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, ChinaKey Laboratory of Brain Science Research & Transformation in Tropical Environment of Hainan Province, Hainan Medical University, Haikou, ChinaDepartment of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, ChinaHainan Health Vocational College, Haikou, ChinaDepartment of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, ChinaKey Laboratory of Brain Science Research & Transformation in Tropical Environment of Hainan Province, Hainan Medical University, Haikou, ChinaDepartment of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, ChinaKey Laboratory of Brain Science Research & Transformation in Tropical Environment of Hainan Province, Hainan Medical University, Haikou, ChinaDepartment of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, ChinaKey Laboratory of Brain Science Research & Transformation in Tropical Environment of Hainan Province, Hainan Medical University, Haikou, ChinaDepartment of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, ChinaKey Laboratory of Brain Science Research & Transformation in Tropical Environment of Hainan Province, Hainan Medical University, Haikou, ChinaDepartment of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, ChinaKey Laboratory of Brain Science Research & Transformation in Tropical Environment of Hainan Province, Hainan Medical University, Haikou, ChinaDepartment of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, ChinaKey Laboratory of Brain Science Research & Transformation in Tropical Environment of Hainan Province, Hainan Medical University, Haikou, ChinaDepartment of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, ChinaKey Laboratory of Brain Science Research & Transformation in Tropical Environment of Hainan Province, Hainan Medical University, Haikou, ChinaDepartment of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, ChinaKey Laboratory of Brain Science Research & Transformation in Tropical Environment of Hainan Province, Hainan Medical University, Haikou, ChinaDepartment of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, ChinaKey Laboratory of Brain Science Research & Transformation in Tropical Environment of Hainan Province, Hainan Medical University, Haikou, ChinaSecreted protein acidic and rich in cysteine (SPARC) is a matricellular protein involved in the extracellular matrix and interactions between cells during neural development of the central nervous system (CNS). Oxidative glutamate toxicity is involved in CNS diseases, including epilepsy, Alzheimer’s disease, and ischemic stroke. However, the molecular mechanism of nerve injury is not fully understood in CNS diseases. Herein, the glutamate-induced nerve damage model was used to explore the molecular mechanisms affecting nerve damage. The levels of SPARC and autophagy were increased in glutamate-induced HT22 hippocampal nerve injury. In summary, the current study confirmed that SPARC regulates autophagy in HT22 hippocampal nerve cells, and its knockdown reduces the glutamate-induced HT22 hippocampal nerve injury by inhibiting autophagy. These findings suggested that SPARC plays a crucial role in nerve injury of CNS diseases.https://www.frontiersin.org/articles/10.3389/fnins.2020.581441/fullSPARCautophagyglutamateHT22epilepsyneurological diseases |