Brain-derived neurotrophic factor protects against acrylamide-induced neuronal and synaptic injury via the TrkB-MAPK-Erk1/2 pathway
Acrylamide has been shown to be neurotoxic. Brain-derived neurotrophic factor (BDNF) can alleviate acrylamide-induced synaptic injury; however, the underlying mechanism remains unclear. In this study, dibutyryl-cyclic adenosine monophosphate-induced mature human neuroblastoma (NB-1) cells were expos...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
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Wolters Kluwer Medknow Publications
2021-01-01
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| Series: | Neural Regeneration Research |
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| Online Access: | http://www.nrronline.org/article.asp?issn=1673-5374;year=2021;volume=16;issue=1;spage=150;epage=157;aulast=Chen |
| _version_ | 1828767605542879232 |
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| author | Xiao Chen Jing-Wei Xiao Peng Cao Yi Zhang Wen-Jian Cai Jia-Yang Song Wei-Min Gao Bin Li |
| author_facet | Xiao Chen Jing-Wei Xiao Peng Cao Yi Zhang Wen-Jian Cai Jia-Yang Song Wei-Min Gao Bin Li |
| author_sort | Xiao Chen |
| collection | DOAJ |
| description | Acrylamide has been shown to be neurotoxic. Brain-derived neurotrophic factor (BDNF) can alleviate acrylamide-induced synaptic injury; however, the underlying mechanism remains unclear. In this study, dibutyryl-cyclic adenosine monophosphate-induced mature human neuroblastoma (NB-1) cells were exposed with 0–100 μg/mL acrylamide for 24–72 hours. Acrylamide decreased cell viability and destroyed synapses. Exposure of co-cultured NB-1 cells and Schwann cells to 0–100 μg/mL acrylamide for 48 hours resulted in upregulated expression of synapsin I and BDNF, suggesting that Schwann cells can activate self-protection of neurons. Under co-culture conditions, activation of the downstream TrkB-MAPK-Erk1/2 pathway strengthened the protective effect. Exogenous BDNF can increase expression of TrkB, Erk1/2, and synapsin I, while exogenous BDNF or the TrkB inhibitor K252a could inhibit these changes. Taken together, Schwann cells may act through the BDNF-TrkB-MAPK-Erk1/2 signaling pathway, indicating that BDNF plays an important role in this process. Therefore, exogenous BDNF may be an effective treatment strategy for acrylamide-induced nerve injury. This study was approved by the Laboratory Animal Welfare and Ethics Committee of the National Institute of Occupational Health and Poison Control, a division of the Chinese Center for Disease Control and Prevention (approval No. EAWE-2017-008) on May 29, 2017. |
| first_indexed | 2024-12-11T07:30:30Z |
| format | Article |
| id | doaj.art-cabccc41591b4f8ca7bddc1752f1f1f6 |
| institution | Directory Open Access Journal |
| issn | 1673-5374 |
| language | English |
| last_indexed | 2024-12-11T07:30:30Z |
| publishDate | 2021-01-01 |
| publisher | Wolters Kluwer Medknow Publications |
| record_format | Article |
| series | Neural Regeneration Research |
| spelling | doaj.art-cabccc41591b4f8ca7bddc1752f1f1f62022-12-22T01:15:51ZengWolters Kluwer Medknow PublicationsNeural Regeneration Research1673-53742021-01-0116115015710.4103/1673-5374.286976Brain-derived neurotrophic factor protects against acrylamide-induced neuronal and synaptic injury via the TrkB-MAPK-Erk1/2 pathwayXiao ChenJing-Wei XiaoPeng CaoYi ZhangWen-Jian CaiJia-Yang SongWei-Min GaoBin LiAcrylamide has been shown to be neurotoxic. Brain-derived neurotrophic factor (BDNF) can alleviate acrylamide-induced synaptic injury; however, the underlying mechanism remains unclear. In this study, dibutyryl-cyclic adenosine monophosphate-induced mature human neuroblastoma (NB-1) cells were exposed with 0–100 μg/mL acrylamide for 24–72 hours. Acrylamide decreased cell viability and destroyed synapses. Exposure of co-cultured NB-1 cells and Schwann cells to 0–100 μg/mL acrylamide for 48 hours resulted in upregulated expression of synapsin I and BDNF, suggesting that Schwann cells can activate self-protection of neurons. Under co-culture conditions, activation of the downstream TrkB-MAPK-Erk1/2 pathway strengthened the protective effect. Exogenous BDNF can increase expression of TrkB, Erk1/2, and synapsin I, while exogenous BDNF or the TrkB inhibitor K252a could inhibit these changes. Taken together, Schwann cells may act through the BDNF-TrkB-MAPK-Erk1/2 signaling pathway, indicating that BDNF plays an important role in this process. Therefore, exogenous BDNF may be an effective treatment strategy for acrylamide-induced nerve injury. This study was approved by the Laboratory Animal Welfare and Ethics Committee of the National Institute of Occupational Health and Poison Control, a division of the Chinese Center for Disease Control and Prevention (approval No. EAWE-2017-008) on May 29, 2017.http://www.nrronline.org/article.asp?issn=1673-5374;year=2021;volume=16;issue=1;spage=150;epage=157;aulast=Chenfactor; injury; pathway; peripheral nerve; protection; protein; regeneration; repair |
| spellingShingle | Xiao Chen Jing-Wei Xiao Peng Cao Yi Zhang Wen-Jian Cai Jia-Yang Song Wei-Min Gao Bin Li Brain-derived neurotrophic factor protects against acrylamide-induced neuronal and synaptic injury via the TrkB-MAPK-Erk1/2 pathway Neural Regeneration Research factor; injury; pathway; peripheral nerve; protection; protein; regeneration; repair |
| title | Brain-derived neurotrophic factor protects against acrylamide-induced neuronal and synaptic injury via the TrkB-MAPK-Erk1/2 pathway |
| title_full | Brain-derived neurotrophic factor protects against acrylamide-induced neuronal and synaptic injury via the TrkB-MAPK-Erk1/2 pathway |
| title_fullStr | Brain-derived neurotrophic factor protects against acrylamide-induced neuronal and synaptic injury via the TrkB-MAPK-Erk1/2 pathway |
| title_full_unstemmed | Brain-derived neurotrophic factor protects against acrylamide-induced neuronal and synaptic injury via the TrkB-MAPK-Erk1/2 pathway |
| title_short | Brain-derived neurotrophic factor protects against acrylamide-induced neuronal and synaptic injury via the TrkB-MAPK-Erk1/2 pathway |
| title_sort | brain derived neurotrophic factor protects against acrylamide induced neuronal and synaptic injury via the trkb mapk erk1 2 pathway |
| topic | factor; injury; pathway; peripheral nerve; protection; protein; regeneration; repair |
| url | http://www.nrronline.org/article.asp?issn=1673-5374;year=2021;volume=16;issue=1;spage=150;epage=157;aulast=Chen |
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