Reduced Expression of Voltage-Gated Sodium Channel Beta 2 Restores Neuronal Injury and Improves Cognitive Dysfunction Induced by Aβ1-42
Voltage-gated sodium channel beta 2 (Nav2.2 or Navβ2, coded by SCN2B mRNA), a gene involved in maintaining normal physiological functions of the prefrontal cortex and hippocampus, might be associated with prefrontal cortex aging and memory decline. This study investigated the effects of Navβ2 in amy...
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| Main Authors: | , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2022-01-01
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| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/2022/3995227 |
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| author | Shan Li Guo-Ji Yan Ya-Xin Tan Lu-Lu Xue Ting-Hua Wang Hao-Ran Zhao Min-Nan Lu Hui-Xiang Zhang Rong Mei Xiao-Han Dong Li-Na Liu Dan Wang Yan-Bin Xiyang |
| author_facet | Shan Li Guo-Ji Yan Ya-Xin Tan Lu-Lu Xue Ting-Hua Wang Hao-Ran Zhao Min-Nan Lu Hui-Xiang Zhang Rong Mei Xiao-Han Dong Li-Na Liu Dan Wang Yan-Bin Xiyang |
| author_sort | Shan Li |
| collection | DOAJ |
| description | Voltage-gated sodium channel beta 2 (Nav2.2 or Navβ2, coded by SCN2B mRNA), a gene involved in maintaining normal physiological functions of the prefrontal cortex and hippocampus, might be associated with prefrontal cortex aging and memory decline. This study investigated the effects of Navβ2 in amyloid-β 1-42- (Aβ1-42-) induced neural injury model and the potential underlying molecular mechanism. The results showed that Navβ2 knockdown restored neuronal viability of Aβ1-42-induced injury in neurons; increased the contents of brain-derived neurotrophic factor (BDNF), enzyme neprilysin (NEP) protein, and NEP enzyme activity; and effectively altered the proportions of the amyloid precursor protein (APP) metabolites including Aβ42, sAPPα, and sAPPβ, thus ameliorating cognitive dysfunction. This may be achieved through regulating NEP transcription and APP metabolism, accelerating Aβ degradation, alleviating neuronal impairment, and regulating BDNF-related signal pathways to repair neuronal synaptic efficiency. This study provides novel evidence indicating that Navβ2 plays crucial roles in the repair of neuronal injury induced by Aβ1-42 both in vivo and in vitro. |
| format | Article |
| id | doaj-art-be126f2ad7754a8eac4ac53e97f71d16 |
| institution | Kabale University |
| issn | 1687-5443 |
| language | English |
| publishDate | 2022-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Neural Plasticity |
| spelling | doaj-art-be126f2ad7754a8eac4ac53e97f71d162025-02-03T05:57:56ZengWileyNeural Plasticity1687-54432022-01-01202210.1155/2022/3995227Reduced Expression of Voltage-Gated Sodium Channel Beta 2 Restores Neuronal Injury and Improves Cognitive Dysfunction Induced by Aβ1-42Shan Li0Guo-Ji Yan1Ya-Xin Tan2Lu-Lu Xue3Ting-Hua Wang4Hao-Ran Zhao5Min-Nan Lu6Hui-Xiang Zhang7Rong Mei8Xiao-Han Dong9Li-Na Liu10Dan Wang11Yan-Bin Xiyang12Institute of NeuroscienceInstitute of NeuroscienceInstitute of NeuroscienceInstitute of NeuroscienceInstitute of NeuroscienceInstitute of NeuroscienceScience and Technology Achievement Incubation CenterInstitute of NeuroscienceDepartment of NeurologyInstitute of NeuroscienceInstitute of NeuroscienceInstitute of NeuroscienceInstitute of NeuroscienceVoltage-gated sodium channel beta 2 (Nav2.2 or Navβ2, coded by SCN2B mRNA), a gene involved in maintaining normal physiological functions of the prefrontal cortex and hippocampus, might be associated with prefrontal cortex aging and memory decline. This study investigated the effects of Navβ2 in amyloid-β 1-42- (Aβ1-42-) induced neural injury model and the potential underlying molecular mechanism. The results showed that Navβ2 knockdown restored neuronal viability of Aβ1-42-induced injury in neurons; increased the contents of brain-derived neurotrophic factor (BDNF), enzyme neprilysin (NEP) protein, and NEP enzyme activity; and effectively altered the proportions of the amyloid precursor protein (APP) metabolites including Aβ42, sAPPα, and sAPPβ, thus ameliorating cognitive dysfunction. This may be achieved through regulating NEP transcription and APP metabolism, accelerating Aβ degradation, alleviating neuronal impairment, and regulating BDNF-related signal pathways to repair neuronal synaptic efficiency. This study provides novel evidence indicating that Navβ2 plays crucial roles in the repair of neuronal injury induced by Aβ1-42 both in vivo and in vitro.http://dx.doi.org/10.1155/2022/3995227 |
| spellingShingle | Shan Li Guo-Ji Yan Ya-Xin Tan Lu-Lu Xue Ting-Hua Wang Hao-Ran Zhao Min-Nan Lu Hui-Xiang Zhang Rong Mei Xiao-Han Dong Li-Na Liu Dan Wang Yan-Bin Xiyang Reduced Expression of Voltage-Gated Sodium Channel Beta 2 Restores Neuronal Injury and Improves Cognitive Dysfunction Induced by Aβ1-42 Neural Plasticity |
| title | Reduced Expression of Voltage-Gated Sodium Channel Beta 2 Restores Neuronal Injury and Improves Cognitive Dysfunction Induced by Aβ1-42 |
| title_full | Reduced Expression of Voltage-Gated Sodium Channel Beta 2 Restores Neuronal Injury and Improves Cognitive Dysfunction Induced by Aβ1-42 |
| title_fullStr | Reduced Expression of Voltage-Gated Sodium Channel Beta 2 Restores Neuronal Injury and Improves Cognitive Dysfunction Induced by Aβ1-42 |
| title_full_unstemmed | Reduced Expression of Voltage-Gated Sodium Channel Beta 2 Restores Neuronal Injury and Improves Cognitive Dysfunction Induced by Aβ1-42 |
| title_short | Reduced Expression of Voltage-Gated Sodium Channel Beta 2 Restores Neuronal Injury and Improves Cognitive Dysfunction Induced by Aβ1-42 |
| title_sort | reduced expression of voltage gated sodium channel beta 2 restores neuronal injury and improves cognitive dysfunction induced by aβ1 42 |
| url | http://dx.doi.org/10.1155/2022/3995227 |
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