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Metabolic reprogramming of inner ear cell line HEI-OC1 after dexamethasone application

INTRODUCTION: One approach to dampen the inflammatory reactions resulting from implantation surgery of cochlear implant hearing aids is to embed dexamethasone into the matrix of the electrode carrier. Possible side effects for sensory cells in the inner ear on the metabolomics have not yet been eval...

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Autores principales: Kather, Michel, Koitzsch, Sabine, Breit, Bernhard, Plontke, Stefan, Kammerer, Bernd, Liebau, Arne
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8144088/
https://www.ncbi.nlm.nih.gov/pubmed/34028607
http://dx.doi.org/10.1007/s11306-021-01799-y
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author Kather, Michel
Koitzsch, Sabine
Breit, Bernhard
Plontke, Stefan
Kammerer, Bernd
Liebau, Arne
author_facet Kather, Michel
Koitzsch, Sabine
Breit, Bernhard
Plontke, Stefan
Kammerer, Bernd
Liebau, Arne
author_sort Kather, Michel
collection PubMed
description INTRODUCTION: One approach to dampen the inflammatory reactions resulting from implantation surgery of cochlear implant hearing aids is to embed dexamethasone into the matrix of the electrode carrier. Possible side effects for sensory cells in the inner ear on the metabolomics have not yet been evaluated. OBJECTIVE: We examined changes in the metabolome of the HEI-OC1 cell line after dexamethasone incubation as a cell model of sensory cells of the inner ear. RESULTS AND CONCLUSION: Untargeted GC–MS-profiling of metabolic alterations after dexamethasone treatment showed that dexamethasone had antithetical effects on the metabolic signature of the cells depending on growth conditions. The differentiated state of HEI-OC1 cells is better suited for elucidating metabolic changes induced by external factors. Dexamethasone treatment of differentiated cells led to an increase in intracellular amino acids and enhanced glucose uptake and β-oxidation in the cells. Increased availability of precursors for glycolysis and ATP production by β-oxidation stabilizes the energy supply in the cells, which could be assumed to be beneficial in coping with cellular stress. We found no negative effects of dexamethasone on the metabolic level, and changes may even prepare sensory cells to better overcome cellular stress following implantation surgery. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s11306-021-01799-y.
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spelling pubmed-81440882021-06-01 Metabolic reprogramming of inner ear cell line HEI-OC1 after dexamethasone application Kather, Michel Koitzsch, Sabine Breit, Bernhard Plontke, Stefan Kammerer, Bernd Liebau, Arne Metabolomics Original Article INTRODUCTION: One approach to dampen the inflammatory reactions resulting from implantation surgery of cochlear implant hearing aids is to embed dexamethasone into the matrix of the electrode carrier. Possible side effects for sensory cells in the inner ear on the metabolomics have not yet been evaluated. OBJECTIVE: We examined changes in the metabolome of the HEI-OC1 cell line after dexamethasone incubation as a cell model of sensory cells of the inner ear. RESULTS AND CONCLUSION: Untargeted GC–MS-profiling of metabolic alterations after dexamethasone treatment showed that dexamethasone had antithetical effects on the metabolic signature of the cells depending on growth conditions. The differentiated state of HEI-OC1 cells is better suited for elucidating metabolic changes induced by external factors. Dexamethasone treatment of differentiated cells led to an increase in intracellular amino acids and enhanced glucose uptake and β-oxidation in the cells. Increased availability of precursors for glycolysis and ATP production by β-oxidation stabilizes the energy supply in the cells, which could be assumed to be beneficial in coping with cellular stress. We found no negative effects of dexamethasone on the metabolic level, and changes may even prepare sensory cells to better overcome cellular stress following implantation surgery. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s11306-021-01799-y. Springer US 2021-05-24 2021 /pmc/articles/PMC8144088/ /pubmed/34028607 http://dx.doi.org/10.1007/s11306-021-01799-y Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Original Article
Kather, Michel
Koitzsch, Sabine
Breit, Bernhard
Plontke, Stefan
Kammerer, Bernd
Liebau, Arne
Metabolic reprogramming of inner ear cell line HEI-OC1 after dexamethasone application
title Metabolic reprogramming of inner ear cell line HEI-OC1 after dexamethasone application
title_full Metabolic reprogramming of inner ear cell line HEI-OC1 after dexamethasone application
title_fullStr Metabolic reprogramming of inner ear cell line HEI-OC1 after dexamethasone application
title_full_unstemmed Metabolic reprogramming of inner ear cell line HEI-OC1 after dexamethasone application
title_short Metabolic reprogramming of inner ear cell line HEI-OC1 after dexamethasone application
title_sort metabolic reprogramming of inner ear cell line hei-oc1 after dexamethasone application
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8144088/
https://www.ncbi.nlm.nih.gov/pubmed/34028607
http://dx.doi.org/10.1007/s11306-021-01799-y
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