Tags

Type your tag names separated by a space and hit enter

Reactive oxygen species regulate miR-17-5p expression via DNA methylation in paraquat-induced nerve cell damage.
Environ Toxicol. 2020 Dec; 35(12):1364-1373.ET

Abstract

There is emerging evidence suggesting that oxidative stress and DNA methylation can alter miRNA expression. However, little is known on the mechanism of miR-17-5p expression changes in paraquat (PQ)-induced nerve cell damage. In the present study, neuro-2a cells were pretreated with antioxidant N-acetylcysteine (NAC) or DNA methylation inhibitor decitabine (DAC), then exposed to different concentrations of PQ, while the expression levels of miR-17-5p were detected by qRT-PCR. Here, it is showed that PQ downregulated the expression of miR-17-5p dose-dependently in neuro-2a cells. The DNA methylation level was upregulated after PQ exposure, while downregulated with the pretreatment of NAC in the above content, detected by 5-mC immunofluorescence technique. The interaction effect of NAC and PQ in alternating DNA methylation level was further confirmed by flow cytometry. NAC and DAC individually had an interaction effect in PQ-induced nerve cell damage. After using NAC, PQ-induced ROS elevation and DNA methylation are reduced, thereby preventing the proapoptotic effect of miR-17-5p. Above all, PQ can induce DNA methylation variations through ROS production, leading to the downregulation of miR-17-5p expression in PQ-induced nerve cell damage.

Authors+Show Affiliations

Department of Health Management, Fujian Health College, Fuzhou, China. Department of Preventive Medicine, Fujian Provincial Key Laboratory of Environment Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou, China.Department of Preventive Medicine, Fujian Provincial Key Laboratory of Environment Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou, China. Key Laboratory of Environment and Health, Universities and Colleges in Fujian, School of Public Health, Fujian Medical University, Fuzhou, China.Department of Preventive Medicine, Fujian Provincial Key Laboratory of Environment Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou, China. Key Laboratory of Environment and Health, Universities and Colleges in Fujian, School of Public Health, Fujian Medical University, Fuzhou, China.Fujian Provincial Center for Adverse Drug Reaction Monitoring, Fujian Provincial Food and Drug Administration, Fuzhou, China.Department of Preventive Medicine, Fujian Provincial Key Laboratory of Environment Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou, China.Department of Preventive Medicine, Fujian Provincial Key Laboratory of Environment Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou, China.Department of Preventive Medicine, Fujian Provincial Key Laboratory of Environment Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou, China.Department of Preventive Medicine, Fujian Provincial Key Laboratory of Environment Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou, China.Department of Preventive Medicine, Fujian Provincial Key Laboratory of Environment Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou, China.Key Laboratory of Environment and Health, Universities and Colleges in Fujian, School of Public Health, Fujian Medical University, Fuzhou, China. Department of Epidemiology and Health Statistics, Fujian Provincial Key Laboratory of Environmental Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou, China.Department of Preventive Medicine, Fujian Provincial Key Laboratory of Environment Factors and Cancer, School of Public Health, Fujian Medical University, Fuzhou, China. Key Laboratory of Environment and Health, Universities and Colleges in Fujian, School of Public Health, Fujian Medical University, Fuzhou, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32691990

Citation

Zhan, Yanting, et al. "Reactive Oxygen Species Regulate miR-17-5p Expression Via DNA Methylation in Paraquat-induced Nerve Cell Damage." Environmental Toxicology, vol. 35, no. 12, 2020, pp. 1364-1373.
Zhan Y, Guo Z, Zheng F, et al. Reactive oxygen species regulate miR-17-5p expression via DNA methylation in paraquat-induced nerve cell damage. Environ Toxicol. 2020;35(12):1364-1373.
Zhan, Y., Guo, Z., Zheng, F., Zhang, Z., Li, K., Wang, Q., Wang, L., Cai, Z., Chen, N., Wu, S., & Li, H. (2020). Reactive oxygen species regulate miR-17-5p expression via DNA methylation in paraquat-induced nerve cell damage. Environmental Toxicology, 35(12), 1364-1373. https://doi.org/10.1002/tox.23001
Zhan Y, et al. Reactive Oxygen Species Regulate miR-17-5p Expression Via DNA Methylation in Paraquat-induced Nerve Cell Damage. Environ Toxicol. 2020;35(12):1364-1373. PubMed PMID: 32691990.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reactive oxygen species regulate miR-17-5p expression via DNA methylation in paraquat-induced nerve cell damage. AU - Zhan,Yanting, AU - Guo,Zhenkun, AU - Zheng,Fuli, AU - Zhang,Zhipeng, AU - Li,Ke, AU - Wang,Qingqing, AU - Wang,Lijin, AU - Cai,Zhipeng, AU - Chen,Nengzhou, AU - Wu,Siying, AU - Li,Huangyuan, Y1 - 2020/07/21/ PY - 2020/03/15/received PY - 2020/06/04/revised PY - 2020/06/28/accepted PY - 2020/7/22/pubmed PY - 2020/11/21/medline PY - 2020/7/22/entrez KW - DNA methylation KW - ROS KW - miR-17-5p KW - neurotoxicity KW - paraquat SP - 1364 EP - 1373 JF - Environmental toxicology JO - Environ Toxicol VL - 35 IS - 12 N2 - There is emerging evidence suggesting that oxidative stress and DNA methylation can alter miRNA expression. However, little is known on the mechanism of miR-17-5p expression changes in paraquat (PQ)-induced nerve cell damage. In the present study, neuro-2a cells were pretreated with antioxidant N-acetylcysteine (NAC) or DNA methylation inhibitor decitabine (DAC), then exposed to different concentrations of PQ, while the expression levels of miR-17-5p were detected by qRT-PCR. Here, it is showed that PQ downregulated the expression of miR-17-5p dose-dependently in neuro-2a cells. The DNA methylation level was upregulated after PQ exposure, while downregulated with the pretreatment of NAC in the above content, detected by 5-mC immunofluorescence technique. The interaction effect of NAC and PQ in alternating DNA methylation level was further confirmed by flow cytometry. NAC and DAC individually had an interaction effect in PQ-induced nerve cell damage. After using NAC, PQ-induced ROS elevation and DNA methylation are reduced, thereby preventing the proapoptotic effect of miR-17-5p. Above all, PQ can induce DNA methylation variations through ROS production, leading to the downregulation of miR-17-5p expression in PQ-induced nerve cell damage. SN - 1522-7278 UR - https://www.unboundmedicine.com/medline/citation/32691990/Reactive_oxygen_species_regulate_miR_17_5p_expression_via_DNA_methylation_in_paraquat_induced_nerve_cell_damage_ L2 - https://doi.org/10.1002/tox.23001 DB - PRIME DP - Unbound Medicine ER -