The interplay between lncRNA NR_030777 and SF3B3 in neuronal damage caused by paraquat
Paraquat (PQ) has been widely acknowledged as an environmental risk factor for Parkinson's disease (PD). However, the interaction between splicing factor and long non-coding RNA (lncRNA) in the process of PQ-induced PD has rarely been studied. Based on previous research, this study focused on s...
| Main Authors: | , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2023-04-01
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| Series: | Ecotoxicology and Environmental Safety |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651323003081 |
| _version_ | 1797851981575880704 |
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| author | Junxiang Wang Yali Weng Yinhan Li Yu Zhang Jinfu Zhou Jianping Tang Xinpei Lin Zhenkun Guo Fuli Zheng Guangxia Yu Wenya Shao Hong Hu Ping Cai Siying Wu Huangyuan Li |
| author_facet | Junxiang Wang Yali Weng Yinhan Li Yu Zhang Jinfu Zhou Jianping Tang Xinpei Lin Zhenkun Guo Fuli Zheng Guangxia Yu Wenya Shao Hong Hu Ping Cai Siying Wu Huangyuan Li |
| author_sort | Junxiang Wang |
| collection | DOAJ |
| description | Paraquat (PQ) has been widely acknowledged as an environmental risk factor for Parkinson's disease (PD). However, the interaction between splicing factor and long non-coding RNA (lncRNA) in the process of PQ-induced PD has rarely been studied. Based on previous research, this study focused on splicing factor 3 subunit 3 (SF3B3) and lncRNA NR_030777. After changing the target gene expression level by lentiviral transfection technology, the related gene expression was detected by western blot and qRT-PCR. The expression of SF3B3 protein was reduced in Neuro-2a cells after PQ exposure, and the reactive oxygen species (ROS) scavenger N-acetylcysteine prevented this decline. Knockdown of SF3B3 reduced the PQ-triggered NR_030777 expression increase, and overexpression of NR_030777 reduced the transcriptional and translational level of Sf3b3. Then, knockdown of SF3B3 exacerbated the PQ-induced decrease in cell viability and aggravated the reduction of tyrosine hydroxylase (TH) protein expression. Overexpressing SF3B3 reversed the reduction of TH expression caused by PQ. Moreover, after intervention with the autophagy inhibitor Bafilomycin A1, LC3B-II protein expression was further increased in Neuro-2a cells with the knockdown of SF3B3, indicating that autophagy was enhanced. In conclusion, PQ modulated the interplay between NR_030777 and SF3B3 through ROS production, thereby impairing autophagic flux and causing neuronal damage. |
| first_indexed | 2024-04-09T19:26:37Z |
| format | Article |
| id | doaj.art-64309b3620784205aab41c96293cb66a |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-04-09T19:26:37Z |
| publishDate | 2023-04-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-64309b3620784205aab41c96293cb66a2023-04-05T08:05:51ZengElsevierEcotoxicology and Environmental Safety0147-65132023-04-01255114804The interplay between lncRNA NR_030777 and SF3B3 in neuronal damage caused by paraquatJunxiang Wang0Yali Weng1Yinhan Li2Yu Zhang3Jinfu Zhou4Jianping Tang5Xinpei Lin6Zhenkun Guo7Fuli Zheng8Guangxia Yu9Wenya Shao10Hong Hu11Ping Cai12Siying Wu13Huangyuan Li14Department of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, ChinaDepartment of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, ChinaDepartment of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, ChinaDepartment of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, ChinaDepartment of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, ChinaDepartment of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, ChinaDepartment of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, ChinaDepartment of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Key Lab of Environment and Health, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Fujian Key Lab of Environmental Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou 350122, ChinaDepartment of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Key Lab of Environment and Health, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Fujian Key Lab of Environmental Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou 350122, ChinaDepartment of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Key Lab of Environment and Health, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Fujian Key Lab of Environmental Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou 350122, ChinaDepartment of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Key Lab of Environment and Health, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Fujian Key Lab of Environmental Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou 350122, ChinaDepartment of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Key Lab of Environment and Health, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Fujian Key Lab of Environmental Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou 350122, ChinaDepartment of Health Inspection and Quarantine, School of Public Health, Fujian Medical University, Fuzhou 350122, ChinaKey Lab of Environment and Health, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Fujian Key Lab of Environmental Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Department of Epidemiology and Health Statistics, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Corresponding authors at: Key Lab of Environment and Health, School of Public Health, Fujian Medical University, Fuzhou 350122, ChinaDepartment of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Key Lab of Environment and Health, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Fujian Key Lab of Environmental Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Corresponding authors at: Key Lab of Environment and Health, School of Public Health, Fujian Medical University, Fuzhou 350122, ChinaParaquat (PQ) has been widely acknowledged as an environmental risk factor for Parkinson's disease (PD). However, the interaction between splicing factor and long non-coding RNA (lncRNA) in the process of PQ-induced PD has rarely been studied. Based on previous research, this study focused on splicing factor 3 subunit 3 (SF3B3) and lncRNA NR_030777. After changing the target gene expression level by lentiviral transfection technology, the related gene expression was detected by western blot and qRT-PCR. The expression of SF3B3 protein was reduced in Neuro-2a cells after PQ exposure, and the reactive oxygen species (ROS) scavenger N-acetylcysteine prevented this decline. Knockdown of SF3B3 reduced the PQ-triggered NR_030777 expression increase, and overexpression of NR_030777 reduced the transcriptional and translational level of Sf3b3. Then, knockdown of SF3B3 exacerbated the PQ-induced decrease in cell viability and aggravated the reduction of tyrosine hydroxylase (TH) protein expression. Overexpressing SF3B3 reversed the reduction of TH expression caused by PQ. Moreover, after intervention with the autophagy inhibitor Bafilomycin A1, LC3B-II protein expression was further increased in Neuro-2a cells with the knockdown of SF3B3, indicating that autophagy was enhanced. In conclusion, PQ modulated the interplay between NR_030777 and SF3B3 through ROS production, thereby impairing autophagic flux and causing neuronal damage.http://www.sciencedirect.com/science/article/pii/S0147651323003081ParaquatParkinson's diseaseSF3B3LncRNA |
| spellingShingle | Junxiang Wang Yali Weng Yinhan Li Yu Zhang Jinfu Zhou Jianping Tang Xinpei Lin Zhenkun Guo Fuli Zheng Guangxia Yu Wenya Shao Hong Hu Ping Cai Siying Wu Huangyuan Li The interplay between lncRNA NR_030777 and SF3B3 in neuronal damage caused by paraquat Ecotoxicology and Environmental Safety Paraquat Parkinson's disease SF3B3 LncRNA |
| title | The interplay between lncRNA NR_030777 and SF3B3 in neuronal damage caused by paraquat |
| title_full | The interplay between lncRNA NR_030777 and SF3B3 in neuronal damage caused by paraquat |
| title_fullStr | The interplay between lncRNA NR_030777 and SF3B3 in neuronal damage caused by paraquat |
| title_full_unstemmed | The interplay between lncRNA NR_030777 and SF3B3 in neuronal damage caused by paraquat |
| title_short | The interplay between lncRNA NR_030777 and SF3B3 in neuronal damage caused by paraquat |
| title_sort | interplay between lncrna nr 030777 and sf3b3 in neuronal damage caused by paraquat |
| topic | Paraquat Parkinson's disease SF3B3 LncRNA |
| url | http://www.sciencedirect.com/science/article/pii/S0147651323003081 |
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