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c-Myb knockdown increases the neomycin-induced damage to hair-cell-like HEI-OC1 cells in vitro
c-Myb is a transcription factor that plays a key role in cell proliferation, differentiation, and apoptosis. It has been reported that c-Myb is expressed within the chicken otic placode, but whether c-Myb exists in the mammalian cochlea, and how it exerts its effects, has not been explored yet. Here...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5253735/ https://www.ncbi.nlm.nih.gov/pubmed/28112219 http://dx.doi.org/10.1038/srep41094 |
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author | Yu, Xiaoyu Liu, Wenwen Fan, Zhaomin Qian, Fuping Zhang, Daogong Han, Yuechen Xu, Lei Sun, Gaoying Qi, Jieyu Zhang, Shasha Tang, Mingliang Li, Jianfeng Chai, Renjie Wang, Haibo |
author_facet | Yu, Xiaoyu Liu, Wenwen Fan, Zhaomin Qian, Fuping Zhang, Daogong Han, Yuechen Xu, Lei Sun, Gaoying Qi, Jieyu Zhang, Shasha Tang, Mingliang Li, Jianfeng Chai, Renjie Wang, Haibo |
author_sort | Yu, Xiaoyu |
collection | PubMed |
description | c-Myb is a transcription factor that plays a key role in cell proliferation, differentiation, and apoptosis. It has been reported that c-Myb is expressed within the chicken otic placode, but whether c-Myb exists in the mammalian cochlea, and how it exerts its effects, has not been explored yet. Here, we investigated the expression of c-Myb in the postnatal mouse cochlea and HEI-OC1 cells and found that c-Myb was expressed in the hair cells (HCs) of mouse cochlea as well as in cultured HEI-OC1 cells. Next, we demonstrated that c-Myb expression was decreased in response to neomycin treatment in both cochlear HCs and HEI-OC1 cells, suggesting an otoprotective role for c-Myb. We then knocked down c-Myb expression with shRNA transfection in HEI-OC1 cells and found that c-Myb knockdown decreased cell viability, increased expression of pro-apoptotic factors, and enhanced cell apoptosis after neomycin insult. Mechanistic studies revealed that c-Myb knockdown increased cellular levels of reactive oxygen species and decreased Bcl-2 expression, both of which are likely to be responsible for the increased sensitivity of c-Myb knockdown cells to neomycin. This study provides evidence that c-Myb might serve as a new target for the prevention of aminoglycoside-induced HC loss. |
format | Online Article Text |
id | pubmed-5253735 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-52537352017-01-24 c-Myb knockdown increases the neomycin-induced damage to hair-cell-like HEI-OC1 cells in vitro Yu, Xiaoyu Liu, Wenwen Fan, Zhaomin Qian, Fuping Zhang, Daogong Han, Yuechen Xu, Lei Sun, Gaoying Qi, Jieyu Zhang, Shasha Tang, Mingliang Li, Jianfeng Chai, Renjie Wang, Haibo Sci Rep Article c-Myb is a transcription factor that plays a key role in cell proliferation, differentiation, and apoptosis. It has been reported that c-Myb is expressed within the chicken otic placode, but whether c-Myb exists in the mammalian cochlea, and how it exerts its effects, has not been explored yet. Here, we investigated the expression of c-Myb in the postnatal mouse cochlea and HEI-OC1 cells and found that c-Myb was expressed in the hair cells (HCs) of mouse cochlea as well as in cultured HEI-OC1 cells. Next, we demonstrated that c-Myb expression was decreased in response to neomycin treatment in both cochlear HCs and HEI-OC1 cells, suggesting an otoprotective role for c-Myb. We then knocked down c-Myb expression with shRNA transfection in HEI-OC1 cells and found that c-Myb knockdown decreased cell viability, increased expression of pro-apoptotic factors, and enhanced cell apoptosis after neomycin insult. Mechanistic studies revealed that c-Myb knockdown increased cellular levels of reactive oxygen species and decreased Bcl-2 expression, both of which are likely to be responsible for the increased sensitivity of c-Myb knockdown cells to neomycin. This study provides evidence that c-Myb might serve as a new target for the prevention of aminoglycoside-induced HC loss. Nature Publishing Group 2017-01-23 /pmc/articles/PMC5253735/ /pubmed/28112219 http://dx.doi.org/10.1038/srep41094 Text en Copyright © 2017, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Yu, Xiaoyu Liu, Wenwen Fan, Zhaomin Qian, Fuping Zhang, Daogong Han, Yuechen Xu, Lei Sun, Gaoying Qi, Jieyu Zhang, Shasha Tang, Mingliang Li, Jianfeng Chai, Renjie Wang, Haibo c-Myb knockdown increases the neomycin-induced damage to hair-cell-like HEI-OC1 cells in vitro |
title | c-Myb knockdown increases the neomycin-induced damage to hair-cell-like HEI-OC1 cells in vitro |
title_full | c-Myb knockdown increases the neomycin-induced damage to hair-cell-like HEI-OC1 cells in vitro |
title_fullStr | c-Myb knockdown increases the neomycin-induced damage to hair-cell-like HEI-OC1 cells in vitro |
title_full_unstemmed | c-Myb knockdown increases the neomycin-induced damage to hair-cell-like HEI-OC1 cells in vitro |
title_short | c-Myb knockdown increases the neomycin-induced damage to hair-cell-like HEI-OC1 cells in vitro |
title_sort | c-myb knockdown increases the neomycin-induced damage to hair-cell-like hei-oc1 cells in vitro |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5253735/ https://www.ncbi.nlm.nih.gov/pubmed/28112219 http://dx.doi.org/10.1038/srep41094 |
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