Sirtuin 1 and Autophagy Attenuate Cisplatin-Induced Hair Cell Death in the Mouse Cochlea and Zebrafish Lateral Line
Cisplatin-induced ototoxicity is one of the major adverse effects in cisplatin chemotherapy, and hearing protective approaches are unavailable in clinical practice. Recent work unveiled a critical role of autophagy in cell survival in various types of hearing loss. Since the excessive activation of...
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Frontiers Media S.A.
2019-01-01
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| Series: | Frontiers in Cellular Neuroscience |
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| Online Access: | https://www.frontiersin.org/article/10.3389/fncel.2018.00515/full |
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| author | Jiaqi Pang Jiaqi Pang Jiaqi Pang Hao Xiong Hao Xiong Ting Zhan Ting Zhan Gui Cheng Haiying Jia Yongyi Ye Zhongwu Su Zhongwu Su Zhongwu Su Hongyu Chen Hanqing Lin Hanqing Lin Hanqing Lin Lan Lai Lan Lai Lan Lai Yongkang Ou Yongkang Ou Yaodong Xu Yaodong Xu Suijun Chen Suijun Chen Qiuhong Huang Qiuhong Huang Maojin Liang Maojin Liang Yuexin Cai Yuexin Cai Xueyuan Zhang Xueyuan Zhang Xiaoding Xu Xiaoding Xu Yiqing Zheng Yiqing Zheng Haidi Yang Haidi Yang |
| author_facet | Jiaqi Pang Jiaqi Pang Jiaqi Pang Hao Xiong Hao Xiong Ting Zhan Ting Zhan Gui Cheng Haiying Jia Yongyi Ye Zhongwu Su Zhongwu Su Zhongwu Su Hongyu Chen Hanqing Lin Hanqing Lin Hanqing Lin Lan Lai Lan Lai Lan Lai Yongkang Ou Yongkang Ou Yaodong Xu Yaodong Xu Suijun Chen Suijun Chen Qiuhong Huang Qiuhong Huang Maojin Liang Maojin Liang Yuexin Cai Yuexin Cai Xueyuan Zhang Xueyuan Zhang Xiaoding Xu Xiaoding Xu Yiqing Zheng Yiqing Zheng Haidi Yang Haidi Yang |
| author_sort | Jiaqi Pang |
| collection | DOAJ |
| description | Cisplatin-induced ototoxicity is one of the major adverse effects in cisplatin chemotherapy, and hearing protective approaches are unavailable in clinical practice. Recent work unveiled a critical role of autophagy in cell survival in various types of hearing loss. Since the excessive activation of autophagy can contribute to apoptotic cell death, whether the activation of autophagy increases or decreases the rate of cell death in CDDP ototoxicity is still being debated. In this study, we showed that CDDP induced activation of autophagy in the auditory cell HEI-OC1 at the early stage. We then used rapamycin, an autophagy activator, to increase the autophagy activity, and found that the cell death significantly decreased after CDDP injury. In contrast, treatment with the autophagy inhibitor 3-methyladenine (3-MA) significantly increased cell death. In accordance with in vitro results, rapamycin alleviated CDDP-induced death of hair cells in zebrafish lateral line and cochlear hair cells in mice. Notably, we found that CDDP-induced increase of Sirtuin 1 (SIRT1) in the HEI-OC1 cells modulated the autophagy function. The specific SIRT1 activator SRT1720 could successfully protect against CDDP-induced cell loss in HEI-OC1 cells, zebrafish lateral line, and mice cochlea. These findings suggest that SIRT1 and autophagy activation can be suggested as potential therapeutic strategies for the treatment of CDDP-induced ototoxicity. |
| first_indexed | 2024-12-11T09:34:23Z |
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| language | English |
| last_indexed | 2024-12-11T09:34:23Z |
| publishDate | 2019-01-01 |
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| series | Frontiers in Cellular Neuroscience |
| spelling | doaj.art-a7cf60cb795d43c7936ab5c6f120acf92022-12-22T01:12:56ZengFrontiers Media S.A.Frontiers in Cellular Neuroscience1662-51022019-01-011210.3389/fncel.2018.00515424781Sirtuin 1 and Autophagy Attenuate Cisplatin-Induced Hair Cell Death in the Mouse Cochlea and Zebrafish Lateral LineJiaqi Pang0Jiaqi Pang1Jiaqi Pang2Hao Xiong3Hao Xiong4Ting Zhan5Ting Zhan6Gui Cheng7Haiying Jia8Yongyi Ye9Zhongwu Su10Zhongwu Su11Zhongwu Su12Hongyu Chen13Hanqing Lin14Hanqing Lin15Hanqing Lin16Lan Lai17Lan Lai18Lan Lai19Yongkang Ou20Yongkang Ou21Yaodong Xu22Yaodong Xu23Suijun Chen24Suijun Chen25Qiuhong Huang26Qiuhong Huang27Maojin Liang28Maojin Liang29Yuexin Cai30Yuexin Cai31Xueyuan Zhang32Xueyuan Zhang33Xiaoding Xu34Xiaoding Xu35Yiqing Zheng36Yiqing Zheng37Haidi Yang38Haidi Yang39Department of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Hearing and Speech Science, Xinhua College, Sun Yat-Sen University, Guangzhou, ChinaGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Hearing and Speech Science, Xinhua College, Sun Yat-Sen University, Guangzhou, ChinaDepartment of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Otolaryngology, The First Affiliated Hospital of Jinan University, Guangzhou, ChinaDepartment of Otolaryngology, The First Affiliated Hospital of Jinan University, Guangzhou, ChinaSchool of Public Health, Sun Yat-sen University, Guangzhou, ChinaDepartment of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Hearing and Speech Science, Xinhua College, Sun Yat-Sen University, Guangzhou, ChinaGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Hearing and Speech Science, Xinhua College, Sun Yat-Sen University, Guangzhou, ChinaDepartment of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Hearing and Speech Science, Xinhua College, Sun Yat-Sen University, Guangzhou, ChinaGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Hearing and Speech Science, Xinhua College, Sun Yat-Sen University, Guangzhou, ChinaGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Hearing and Speech Science, Xinhua College, Sun Yat-Sen University, Guangzhou, ChinaDepartment of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Hearing and Speech Science, Xinhua College, Sun Yat-Sen University, Guangzhou, ChinaDepartment of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Hearing and Speech Science, Xinhua College, Sun Yat-Sen University, Guangzhou, ChinaDepartment of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Hearing and Speech Science, Xinhua College, Sun Yat-Sen University, Guangzhou, ChinaDepartment of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Hearing and Speech Science, Xinhua College, Sun Yat-Sen University, Guangzhou, ChinaDepartment of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Hearing and Speech Science, Xinhua College, Sun Yat-Sen University, Guangzhou, ChinaDepartment of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Hearing and Speech Science, Xinhua College, Sun Yat-Sen University, Guangzhou, ChinaGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaRNA Biomedical Institute, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Hearing and Speech Science, Xinhua College, Sun Yat-Sen University, Guangzhou, ChinaDepartment of Otolaryngology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, ChinaDepartment of Hearing and Speech Science, Xinhua College, Sun Yat-Sen University, Guangzhou, ChinaCisplatin-induced ototoxicity is one of the major adverse effects in cisplatin chemotherapy, and hearing protective approaches are unavailable in clinical practice. Recent work unveiled a critical role of autophagy in cell survival in various types of hearing loss. Since the excessive activation of autophagy can contribute to apoptotic cell death, whether the activation of autophagy increases or decreases the rate of cell death in CDDP ototoxicity is still being debated. In this study, we showed that CDDP induced activation of autophagy in the auditory cell HEI-OC1 at the early stage. We then used rapamycin, an autophagy activator, to increase the autophagy activity, and found that the cell death significantly decreased after CDDP injury. In contrast, treatment with the autophagy inhibitor 3-methyladenine (3-MA) significantly increased cell death. In accordance with in vitro results, rapamycin alleviated CDDP-induced death of hair cells in zebrafish lateral line and cochlear hair cells in mice. Notably, we found that CDDP-induced increase of Sirtuin 1 (SIRT1) in the HEI-OC1 cells modulated the autophagy function. The specific SIRT1 activator SRT1720 could successfully protect against CDDP-induced cell loss in HEI-OC1 cells, zebrafish lateral line, and mice cochlea. These findings suggest that SIRT1 and autophagy activation can be suggested as potential therapeutic strategies for the treatment of CDDP-induced ototoxicity.https://www.frontiersin.org/article/10.3389/fncel.2018.00515/fullSIRT1autophagycisplatincell deathototoxicity |
| spellingShingle | Jiaqi Pang Jiaqi Pang Jiaqi Pang Hao Xiong Hao Xiong Ting Zhan Ting Zhan Gui Cheng Haiying Jia Yongyi Ye Zhongwu Su Zhongwu Su Zhongwu Su Hongyu Chen Hanqing Lin Hanqing Lin Hanqing Lin Lan Lai Lan Lai Lan Lai Yongkang Ou Yongkang Ou Yaodong Xu Yaodong Xu Suijun Chen Suijun Chen Qiuhong Huang Qiuhong Huang Maojin Liang Maojin Liang Yuexin Cai Yuexin Cai Xueyuan Zhang Xueyuan Zhang Xiaoding Xu Xiaoding Xu Yiqing Zheng Yiqing Zheng Haidi Yang Haidi Yang Sirtuin 1 and Autophagy Attenuate Cisplatin-Induced Hair Cell Death in the Mouse Cochlea and Zebrafish Lateral Line Frontiers in Cellular Neuroscience SIRT1 autophagy cisplatin cell death ototoxicity |
| title | Sirtuin 1 and Autophagy Attenuate Cisplatin-Induced Hair Cell Death in the Mouse Cochlea and Zebrafish Lateral Line |
| title_full | Sirtuin 1 and Autophagy Attenuate Cisplatin-Induced Hair Cell Death in the Mouse Cochlea and Zebrafish Lateral Line |
| title_fullStr | Sirtuin 1 and Autophagy Attenuate Cisplatin-Induced Hair Cell Death in the Mouse Cochlea and Zebrafish Lateral Line |
| title_full_unstemmed | Sirtuin 1 and Autophagy Attenuate Cisplatin-Induced Hair Cell Death in the Mouse Cochlea and Zebrafish Lateral Line |
| title_short | Sirtuin 1 and Autophagy Attenuate Cisplatin-Induced Hair Cell Death in the Mouse Cochlea and Zebrafish Lateral Line |
| title_sort | sirtuin 1 and autophagy attenuate cisplatin induced hair cell death in the mouse cochlea and zebrafish lateral line |
| topic | SIRT1 autophagy cisplatin cell death ototoxicity |
| url | https://www.frontiersin.org/article/10.3389/fncel.2018.00515/full |
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