Functionally and morphologically damaged mitochondria observed in auditory cells under senescence-inducing stress
We aimed at determining the mitochondrial function in premature senescence model of auditory cells. Short exposure to H(2)O(2) (1 h, 0.1 mM) induced premature cellular senescence in House Ear Institute-Organ of Corti 1 auditory cells. The transmission electron microscopy analysis revealed that damag...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5445612/ https://www.ncbi.nlm.nih.gov/pubmed/28649420 http://dx.doi.org/10.1038/s41514-017-0002-2 |
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author | Kamogashira, Teru Hayashi, Ken Fujimoto, Chisato Iwasaki, Shinichi Yamasoba, Tatsuya |
author_facet | Kamogashira, Teru Hayashi, Ken Fujimoto, Chisato Iwasaki, Shinichi Yamasoba, Tatsuya |
author_sort | Kamogashira, Teru |
collection | PubMed |
description | We aimed at determining the mitochondrial function in premature senescence model of auditory cells. Short exposure to H(2)O(2) (1 h, 0.1 mM) induced premature cellular senescence in House Ear Institute-Organ of Corti 1 auditory cells. The transmission electron microscopy analysis revealed that damaged mitochondria and autophagosomes containing dense organelles appeared in the auditory cells after short exposure to H(2)O(2). The branch and junction parameters of the skeletonized image of the mitochondria were found to decrease significantly in H(2)O(2)-treated cells. A branched reticulum of tubules was poorly formed, featuring coexistence of numerous tiny clusters along with few relatively large entities in the H(2)O(2)-treated cells. In terms of bioenergetics, H(2)O(2)-treatment led to the dose-dependent decrease in mitochondrial membrane potential in the auditory cells. The fragmented mitochondria (fusion < fission) were in a low potential. In addition, the potential of hyperfused mitochondria (fusion > fission) was slightly lower than the control cells. The short-time exposure of live auditory cells to H(2)O(2) damaged the mitochondrial respiratory capacity without any effect on the baseline ATP production rates. The vulnerability of the mitochondrial membrane potential to the uncoupling reagent was increased after H(2)O(2) treatment. Our findings indicated that the mitochondrial dysfunction due to the decline in the O(2) consumption rate should be the first event of premature senescence process in the auditory cells, resulting in the imbalance of mitochondrial fusion/fission and the collapse of the mitochondrial network. |
format | Online Article Text |
id | pubmed-5445612 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-54456122017-06-23 Functionally and morphologically damaged mitochondria observed in auditory cells under senescence-inducing stress Kamogashira, Teru Hayashi, Ken Fujimoto, Chisato Iwasaki, Shinichi Yamasoba, Tatsuya NPJ Aging Mech Dis Article We aimed at determining the mitochondrial function in premature senescence model of auditory cells. Short exposure to H(2)O(2) (1 h, 0.1 mM) induced premature cellular senescence in House Ear Institute-Organ of Corti 1 auditory cells. The transmission electron microscopy analysis revealed that damaged mitochondria and autophagosomes containing dense organelles appeared in the auditory cells after short exposure to H(2)O(2). The branch and junction parameters of the skeletonized image of the mitochondria were found to decrease significantly in H(2)O(2)-treated cells. A branched reticulum of tubules was poorly formed, featuring coexistence of numerous tiny clusters along with few relatively large entities in the H(2)O(2)-treated cells. In terms of bioenergetics, H(2)O(2)-treatment led to the dose-dependent decrease in mitochondrial membrane potential in the auditory cells. The fragmented mitochondria (fusion < fission) were in a low potential. In addition, the potential of hyperfused mitochondria (fusion > fission) was slightly lower than the control cells. The short-time exposure of live auditory cells to H(2)O(2) damaged the mitochondrial respiratory capacity without any effect on the baseline ATP production rates. The vulnerability of the mitochondrial membrane potential to the uncoupling reagent was increased after H(2)O(2) treatment. Our findings indicated that the mitochondrial dysfunction due to the decline in the O(2) consumption rate should be the first event of premature senescence process in the auditory cells, resulting in the imbalance of mitochondrial fusion/fission and the collapse of the mitochondrial network. Nature Publishing Group UK 2017-01-25 /pmc/articles/PMC5445612/ /pubmed/28649420 http://dx.doi.org/10.1038/s41514-017-0002-2 Text en © The Author(s) 2017 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 Kamogashira, Teru Hayashi, Ken Fujimoto, Chisato Iwasaki, Shinichi Yamasoba, Tatsuya Functionally and morphologically damaged mitochondria observed in auditory cells under senescence-inducing stress |
title | Functionally and morphologically damaged mitochondria observed in auditory cells under senescence-inducing stress |
title_full | Functionally and morphologically damaged mitochondria observed in auditory cells under senescence-inducing stress |
title_fullStr | Functionally and morphologically damaged mitochondria observed in auditory cells under senescence-inducing stress |
title_full_unstemmed | Functionally and morphologically damaged mitochondria observed in auditory cells under senescence-inducing stress |
title_short | Functionally and morphologically damaged mitochondria observed in auditory cells under senescence-inducing stress |
title_sort | functionally and morphologically damaged mitochondria observed in auditory cells under senescence-inducing stress |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5445612/ https://www.ncbi.nlm.nih.gov/pubmed/28649420 http://dx.doi.org/10.1038/s41514-017-0002-2 |
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