Toxic Effects of 3,3′-Iminodipropionitrile on Vestibular System in Adult C57BL/6J Mice In Vivo
The utricle is one of the five sensory organs in the mammalian vestibular system, and while the utricle has a limited ability to repair itself, this is not sufficient for the recovery of vestibular function after hair cell (HC) loss induced by ototoxic drugs. In order to further explore the possible...
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Published in | Journal of neural transplantation & plasticity Vol. 2020; no. 2020; pp. 1 - 11 |
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Main Authors | , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Cairo, Egypt
Hindawi Publishing Corporation
2020
Hindawi Hindawi Limited Wiley |
Subjects | |
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Abstract | The utricle is one of the five sensory organs in the mammalian vestibular system, and while the utricle has a limited ability to repair itself, this is not sufficient for the recovery of vestibular function after hair cell (HC) loss induced by ototoxic drugs. In order to further explore the possible self-recovery mechanism of the adult mouse vestibular system, we established a reliable utricle epithelium injury model for studying the regeneration of HCs and examined the toxic effects of 3,3′-iminodiproprionitrile (IDPN) on the utricle in vivo in C57BL/6J mice, which is one of the most commonly used strains in inner ear research. This work focused on the epithelial cell loss, vestibular dysfunction, and spontaneous cell regeneration after IDPN administration. HC loss and supporting cell (SC) loss after IDPN treatment was dose-dependent and resulted in dysfunction of the vestibular system, as indicated by the swim test and the rotating vestibular ocular reflex (VOR) test. EdU-positive SCs were observed only in severely injured utricles wherein above 47% SCs were dead. No EdU-positive HCs were observed in either control or injured utricles. RT-qPCR showed transient upregulation of Hes5 and Hey1 and fluctuating upregulation of Axin2 and β-catenin after IDPN administration. We conclude that a single intraperitoneal injection of IDPN is a practical way to establish an injured utricle model in adult C57BL/6J mice in vivo. We observed activation of Notch and Wnt signaling during the limited spontaneous HC regeneration after vestibular sensory epithelium damage, and such signaling might act as the promoting factors for tissue self-repair in the inner ear. |
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AbstractList | The utricle is one of the five sensory organs in the mammalian vestibular system, and while the utricle has a limited ability to repair itself, this is not sufficient for the recovery of vestibular function after hair cell (HC) loss induced by ototoxic drugs. In order to further explore the possible self-recovery mechanism of the adult mouse vestibular system, we established a reliable utricle epithelium injury model for studying the regeneration of HCs and examined the toxic effects of 3,3′-iminodiproprionitrile (IDPN) on the utricle in vivo in C57BL/6J mice, which is one of the most commonly used strains in inner ear research. This work focused on the epithelial cell loss, vestibular dysfunction, and spontaneous cell regeneration after IDPN administration. HC loss and supporting cell (SC) loss after IDPN treatment was dose-dependent and resulted in dysfunction of the vestibular system, as indicated by the swim test and the rotating vestibular ocular reflex (VOR) test. EdU-positive SCs were observed only in severely injured utricles wherein above 47% SCs were dead. No EdU-positive HCs were observed in either control or injured utricles. RT-qPCR showed transient upregulation of Hes5 and Hey1 and fluctuating upregulation of Axin2 and β-catenin after IDPN administration. We conclude that a single intraperitoneal injection of IDPN is a practical way to establish an injured utricle model in adult C57BL/6J mice in vivo. We observed activation of Notch and Wnt signaling during the limited spontaneous HC regeneration after vestibular sensory epithelium damage, and such signaling might act as the promoting factors for tissue self-repair in the inner ear. The utricle is one of the five sensory organs in the mammalian vestibular system, and while the utricle has a limited ability to repair itself, this is not sufficient for the recovery of vestibular function after hair cell (HC) loss induced by ototoxic drugs. In order to further explore the possible self-recovery mechanism of the adult mouse vestibular system, we established a reliable utricle epithelium injury model for studying the regeneration of HCs and examined the toxic effects of 3,3'-iminodiproprionitrile (IDPN) on the utricle in vivo in C57BL/6J mice, which is one of the most commonly used strains in inner ear research. This work focused on the epithelial cell loss, vestibular dysfunction, and spontaneous cell regeneration after IDPN administration. HC loss and supporting cell (SC) loss after IDPN treatment was dose-dependent and resulted in dysfunction of the vestibular system, as indicated by the swim test and the rotating vestibular ocular reflex (VOR) test. EdU-positive SCs were observed only in severely injured utricles wherein above 47% SCs were dead. No EdU-positive HCs were observed in either control or injured utricles. RT-qPCR showed transient upregulation of Hes5 and Hey1 and fluctuating upregulation of Axin2 and [beta]-catenin after IDPN administration. We conclude that a single intraperitoneal injection of IDPN is a practical way to establish an injured utricle model in adult C57BL/6J mice in vivo. We observed activation of Notch and Wnt signaling during the limited spontaneous HC regeneration after vestibular sensory epithelium damage, and such signaling might act as the promoting factors for tissue self-repair in the inner ear. The utricle is one of the five sensory organs in the mammalian vestibular system, and while the utricle has a limited ability to repair itself, this is not sufficient for the recovery of vestibular function after hair cell (HC) loss induced by ototoxic drugs. In order to further explore the possible self-recovery mechanism of the adult mouse vestibular system, we established a reliable utricle epithelium injury model for studying the regeneration of HCs and examined the toxic effects of 3,3′-iminodiproprionitrile (IDPN) on the utricle in vivo in C57BL/6J mice, which is one of the most commonly used strains in inner ear research. This work focused on the epithelial cell loss, vestibular dysfunction, and spontaneous cell regeneration after IDPN administration. HC loss and supporting cell (SC) loss after IDPN treatment was dose-dependent and resulted in dysfunction of the vestibular system, as indicated by the swim test and the rotating vestibular ocular reflex (VOR) test. EdU-positive SCs were observed only in severely injured utricles wherein above 47% SCs were dead. No EdU-positive HCs were observed in either control or injured utricles. RT-qPCR showed transient upregulation of Hes5 and Hey1 and fluctuating upregulation of Axin2 and β-catenin after IDPN administration. We conclude that a single intraperitoneal injection of IDPN is a practical way to establish an injured utricle model in adult C57BL/6J mice in vivo . We observed activation of Notch and Wnt signaling during the limited spontaneous HC regeneration after vestibular sensory epithelium damage, and such signaling might act as the promoting factors for tissue self-repair in the inner ear. The utricle is one of the five sensory organs in the mammalian vestibular system, and while the utricle has a limited ability to repair itself, this is not sufficient for the recovery of vestibular function after hair cell (HC) loss induced by ototoxic drugs. In order to further explore the possible self-recovery mechanism of the adult mouse vestibular system, we established a reliable utricle epithelium injury model for studying the regeneration of HCs and examined the toxic effects of 3,3 ′ -iminodiproprionitrile (IDPN) on the utricle in vivo in C57BL/6J mice, which is one of the most commonly used strains in inner ear research. This work focused on the epithelial cell loss, vestibular dysfunction, and spontaneous cell regeneration after IDPN administration. HC loss and supporting cell (SC) loss after IDPN treatment was dose-dependent and resulted in dysfunction of the vestibular system, as indicated by the swim test and the rotating vestibular ocular reflex (VOR) test. EdU-positive SCs were observed only in severely injured utricles wherein above 47% SCs were dead. No EdU-positive HCs were observed in either control or injured utricles. RT-qPCR showed transient upregulation of Hes5 and Hey1 and fluctuating upregulation of Axin2 and β-catenin after IDPN administration. We conclude that a single intraperitoneal injection of IDPN is a practical way to establish an injured utricle model in adult C57BL/6J mice in vivo . We observed activation of Notch and Wnt signaling during the limited spontaneous HC regeneration after vestibular sensory epithelium damage, and such signaling might act as the promoting factors for tissue self-repair in the inner ear. |
Audience | Academic |
Author | You, Dan Li, Wenyan Liu, Liman Jiang, Hui Chen, Fangyi Lu, Xiaoling Li, Huawei Chen, Yan Yu, Huiqian Zeng, Shan Wang, Jinghan Ni, Wenli Wang, Yunfeng Wu, Jingfang |
AuthorAffiliation | 3 The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China 2 Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China 4 Department of Biomedical Engineering, Southern University of Science and Technology, Shenzhen, Guangdong 518055, China 1 ENT Institute and Otorhinolaryngology Department of Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200031, China |
AuthorAffiliation_xml | – name: 1 ENT Institute and Otorhinolaryngology Department of Affiliated Eye and ENT Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200031, China – name: 2 Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China – name: 4 Department of Biomedical Engineering, Southern University of Science and Technology, Shenzhen, Guangdong 518055, China – name: 3 The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China |
Author_xml | – sequence: 1 fullname: Wu, Jingfang – sequence: 2 fullname: Li, Huawei – sequence: 3 fullname: Wang, Yunfeng – sequence: 4 fullname: Chen, Yan – sequence: 5 fullname: Li, Wenyan – sequence: 6 fullname: Yu, Huiqian – sequence: 7 fullname: Liu, Liman – sequence: 8 fullname: Lu, Xiaoling – sequence: 9 fullname: Wang, Jinghan – sequence: 10 fullname: You, Dan – sequence: 11 fullname: Jiang, Hui – sequence: 12 fullname: Ni, Wenli – sequence: 13 fullname: Zeng, Shan – sequence: 14 fullname: Chen, Fangyi |
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CitedBy_id | crossref_primary_10_3757_jser_80_216 crossref_primary_10_3389_fnmol_2022_854635 crossref_primary_10_7554_eLife_88819_3 crossref_primary_10_7554_eLife_88819 |
Cites_doi | 10.1002/tox.22286 10.1002/cne.23625 10.1007/s12035-015-9545-z 10.1093/toxsci/kfp082 10.1007/s00401-003-0744-8 10.1016/S0892-0362(96)00216-4 10.1006/taap.1993.1238 10.1093/toxsci/kfl186 10.1016/j.heares.2008.08.010 10.1523/JNEUROSCI.1709-12.2012 10.1007/s10162-007-0106-7 10.1002/cne.1357 10.1093/toxsci/kfp043 10.1038/cddis.2016.35 10.1038/nprot.2009.204 10.1097/TA.0000000000000804 10.3390/cancers11040555 10.1007/s10162-018-00687-y 10.1007/s10162-009-0162-2 10.1523/JNEUROSCI.3336-13.2014 10.1016/j.neulet.2018.12.036 10.1126/science.7839150 10.1016/0378-5955(94)90090-6 10.1242/dev.126.8.1581 10.1073/pnas.1202774109 10.1523/JNEUROSCI.6366-10.2011 10.1242/dev.080358 10.1152/jn.00428.2004 10.1096/fj.03-0035fje 10.1016/j.heares.2010.03.085 10.1038/nrm2009 10.1007/s10162-013-0414-z 10.1016/0892-0362(89)90028-7 10.1078/0940-2993-00312 |
ContentType | Journal Article |
Copyright | Copyright © 2020 Shan Zeng et al. COPYRIGHT 2020 Hindawi Limited Copyright © 2020 Shan Zeng et al. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Copyright © 2020 Shan Zeng et al. 2020 |
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References | 22 23 24 25 26 27 28 29 30 10 32 (8) 1994; 15 11 33 12 34 13 35 14 15 16 17 18 19 (31) 1999; 126 1 2 3 4 5 6 7 9 20 21 |
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Snippet | The utricle is one of the five sensory organs in the mammalian vestibular system, and while the utricle has a limited ability to repair itself, this is not... |
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SubjectTerms | Antibodies EDTA Experiments Eye movements Gene expression House mouse Laboratory animals Software Somatotropin Swimming |
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Title | Toxic Effects of 3,3′-Iminodipropionitrile on Vestibular System in Adult C57BL/6J Mice In Vivo |
URI | https://search.emarefa.net/detail/BIM-1202631 https://dx.doi.org/10.1155/2020/1823454 https://www.proquest.com/docview/2423433783/abstract/ https://pubmed.ncbi.nlm.nih.gov/PMC7354661 https://doaj.org/article/c65734e9c8154a8d8c4e2401ebf5375e |
Volume | 2020 |
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