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Crosstalk between Mitochondrial Fission and Oxidative Stress in Paraquat-Induced Apoptosis in Mouse Alveolar Type II Cells.
Int J Biol Sci. 2017; 13(7):888-900.IJ

Abstract

Paraquat (PQ), as a highly effective and nonselective herbicide, induces cell apoptosis through generation of superoxide anions which forms reactive oxygen species (ROS). Mitochondria, as regulators for cellular redox signaling, have been proved to play an important role in PQ-induced cell apoptosis. This study aimed to evaluate whether and how mitochondrial fission interacts with oxidative stress in PQ-induced apoptosis in mouse alveolar type II (AT-II) cells. Firstly, we demonstrated that PQ promoted apoptosis and release of cytochrome-c (Cyt-c). Furthermore, we showed that PQ broke down mitochondrial network, enhanced the expression of fission-related proteins, increased Drp1 mitochondrial translocation while decreased the expression of fusion-related proteins in AT-II cells. Besides, inhibiting mitochondrial fission using mdivi-1, a selective inhibitor of Drp1, markedly attenuated PQ-induced apoptosis, release of Cyt-c and the generation of ROS. These results indicate that mitochondrial fission involves in PQ-induced apoptosis. Further study demonstrated that antioxidant ascorbic acid inhibited Drp1 mitochondrial translocation, mitochondrial fission and attenuated PQ-induced apoptosis. Overall, our findings suggest that mitochondrial fission interplays with ROS in PQ-induced apoptosis in mouse AT-II cells and mitochondrial fission could serve as a potential therapeutic target in PQ poisoning.

Authors+Show Affiliations

Emergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China. Wenzhou Municipal Key Laboratory of Emergency, Critical care, and Disaster Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.Emergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China. Wenzhou Municipal Key Laboratory of Emergency, Critical care, and Disaster Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.Emergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China. Wenzhou Municipal Key Laboratory of Emergency, Critical care, and Disaster Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.Emergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.Emergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.Department of Microbiology and immunology, School of Laboratory Medicine, Wenzhou Medical University, Wenzhou 325000, China. Key Lab of Laboratory Medicine, Ministry of Education of China, Wenzhou 325000, China.Emergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China. Wenzhou Municipal Key Laboratory of Emergency, Critical care, and Disaster Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.Emergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China. Wenzhou Municipal Key Laboratory of Emergency, Critical care, and Disaster Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.Emergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.Emergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.Emergency Department, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China. Wenzhou Municipal Key Laboratory of Emergency, Critical care, and Disaster Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

28808421

Citation

Zhao, Guangju, et al. "Crosstalk Between Mitochondrial Fission and Oxidative Stress in Paraquat-Induced Apoptosis in Mouse Alveolar Type II Cells." International Journal of Biological Sciences, vol. 13, no. 7, 2017, pp. 888-900.
Zhao G, Cao K, Xu C, et al. Crosstalk between Mitochondrial Fission and Oxidative Stress in Paraquat-Induced Apoptosis in Mouse Alveolar Type II Cells. Int J Biol Sci. 2017;13(7):888-900.
Zhao, G., Cao, K., Xu, C., Sun, A., Lu, W., Zheng, Y., Li, H., Hong, G., Wu, B., Qiu, Q., & Lu, Z. (2017). Crosstalk between Mitochondrial Fission and Oxidative Stress in Paraquat-Induced Apoptosis in Mouse Alveolar Type II Cells. International Journal of Biological Sciences, 13(7), 888-900. https://doi.org/10.7150/ijbs.18468
Zhao G, et al. Crosstalk Between Mitochondrial Fission and Oxidative Stress in Paraquat-Induced Apoptosis in Mouse Alveolar Type II Cells. Int J Biol Sci. 2017;13(7):888-900. PubMed PMID: 28808421.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Crosstalk between Mitochondrial Fission and Oxidative Stress in Paraquat-Induced Apoptosis in Mouse Alveolar Type II Cells. AU - Zhao,Guangju, AU - Cao,Kaiqiang, AU - Xu,Changqin, AU - Sun,Aifang, AU - Lu,Wang, AU - Zheng,Yi, AU - Li,Haixiao, AU - Hong,Guangliang, AU - Wu,Bing, AU - Qiu,Qiaomeng, AU - Lu,Zhongqiu, Y1 - 2017/07/07/ PY - 2016/11/23/received PY - 2017/03/10/accepted PY - 2017/8/16/entrez PY - 2017/8/16/pubmed PY - 2018/5/5/medline KW - apoptosis KW - mitochondrial fission KW - oxidative stress KW - paraquat KW - reactive oxygen species. SP - 888 EP - 900 JF - International journal of biological sciences JO - Int. J. Biol. Sci. VL - 13 IS - 7 N2 - Paraquat (PQ), as a highly effective and nonselective herbicide, induces cell apoptosis through generation of superoxide anions which forms reactive oxygen species (ROS). Mitochondria, as regulators for cellular redox signaling, have been proved to play an important role in PQ-induced cell apoptosis. This study aimed to evaluate whether and how mitochondrial fission interacts with oxidative stress in PQ-induced apoptosis in mouse alveolar type II (AT-II) cells. Firstly, we demonstrated that PQ promoted apoptosis and release of cytochrome-c (Cyt-c). Furthermore, we showed that PQ broke down mitochondrial network, enhanced the expression of fission-related proteins, increased Drp1 mitochondrial translocation while decreased the expression of fusion-related proteins in AT-II cells. Besides, inhibiting mitochondrial fission using mdivi-1, a selective inhibitor of Drp1, markedly attenuated PQ-induced apoptosis, release of Cyt-c and the generation of ROS. These results indicate that mitochondrial fission involves in PQ-induced apoptosis. Further study demonstrated that antioxidant ascorbic acid inhibited Drp1 mitochondrial translocation, mitochondrial fission and attenuated PQ-induced apoptosis. Overall, our findings suggest that mitochondrial fission interplays with ROS in PQ-induced apoptosis in mouse AT-II cells and mitochondrial fission could serve as a potential therapeutic target in PQ poisoning. SN - 1449-2288 UR - https://www.unboundmedicine.com/medline/citation/28808421/Crosstalk_between_Mitochondrial_Fission_and_Oxidative_Stress_in_Paraquat_Induced_Apoptosis_in_Mouse_Alveolar_Type_II_Cells_ L2 - http://www.ijbs.com/v13p0888.htm DB - PRIME DP - Unbound Medicine ER -