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Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress
BACKGROUND: To analyze mechanisms of action of glucocorticoid treatment for endoplasmic reticulum stress (ERS) in sensorineural hearing loss (SNHL), we aimed to evaluate the expression and activation status of the protein kinase RNA-like ER kinase (PERK)–C/EBP homologous protein (CHOP) pathway, whic...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
De Gruyter
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8253451/ https://www.ncbi.nlm.nih.gov/pubmed/34250248 http://dx.doi.org/10.1515/biol-2021-0057 |
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author | Liu, Zhibiao Fei, Bing Xie, Lisheng Liu, Jin Chen, Xiaorui Zhu, Wenyan Lv, Lingyun Ma, Wei Gao, Ziwen Hou, Jie She, Wandong |
author_facet | Liu, Zhibiao Fei, Bing Xie, Lisheng Liu, Jin Chen, Xiaorui Zhu, Wenyan Lv, Lingyun Ma, Wei Gao, Ziwen Hou, Jie She, Wandong |
author_sort | Liu, Zhibiao |
collection | PubMed |
description | BACKGROUND: To analyze mechanisms of action of glucocorticoid treatment for endoplasmic reticulum stress (ERS) in sensorineural hearing loss (SNHL), we aimed to evaluate the expression and activation status of the protein kinase RNA-like ER kinase (PERK)–C/EBP homologous protein (CHOP) pathway, which is the major pathway in the ERS. METHODS: In the present study, we established an in vitro ERS model using tunicamycin-treated hair-cell-like HEI-OC1 cells. The effect of dexamethasone on proliferation inhibition, apoptosis, and ATF4–CHOP pathway in HEI-OC1 cells was examined by CCK-8 assay, flow cytometry, western blotting, and reverse transcription PCR, respectively. RESULTS: In HEI-OC1 cells, dexamethasone was shown to significantly reduce the tunicamycin-induced expression of ATF4 and CHOP in the context of sustained viability and proliferation, a therapeutic effect that was reversible by co-treatment with a glucocorticoid antagonist. CONCLUSION: Dexamethasone can protect hair-cell-like HEI-OC1 cells from ERS damage, which may be one of the mechanisms of action for GCs in SNHL treatment. |
format | Online Article Text |
id | pubmed-8253451 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | De Gruyter |
record_format | MEDLINE/PubMed |
spelling | pubmed-82534512021-07-08 Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress Liu, Zhibiao Fei, Bing Xie, Lisheng Liu, Jin Chen, Xiaorui Zhu, Wenyan Lv, Lingyun Ma, Wei Gao, Ziwen Hou, Jie She, Wandong Open Life Sci Research Article BACKGROUND: To analyze mechanisms of action of glucocorticoid treatment for endoplasmic reticulum stress (ERS) in sensorineural hearing loss (SNHL), we aimed to evaluate the expression and activation status of the protein kinase RNA-like ER kinase (PERK)–C/EBP homologous protein (CHOP) pathway, which is the major pathway in the ERS. METHODS: In the present study, we established an in vitro ERS model using tunicamycin-treated hair-cell-like HEI-OC1 cells. The effect of dexamethasone on proliferation inhibition, apoptosis, and ATF4–CHOP pathway in HEI-OC1 cells was examined by CCK-8 assay, flow cytometry, western blotting, and reverse transcription PCR, respectively. RESULTS: In HEI-OC1 cells, dexamethasone was shown to significantly reduce the tunicamycin-induced expression of ATF4 and CHOP in the context of sustained viability and proliferation, a therapeutic effect that was reversible by co-treatment with a glucocorticoid antagonist. CONCLUSION: Dexamethasone can protect hair-cell-like HEI-OC1 cells from ERS damage, which may be one of the mechanisms of action for GCs in SNHL treatment. De Gruyter 2021-07-01 /pmc/articles/PMC8253451/ /pubmed/34250248 http://dx.doi.org/10.1515/biol-2021-0057 Text en © 2021 Zhibiao Liu et al., published by De Gruyter https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 International License. |
spellingShingle | Research Article Liu, Zhibiao Fei, Bing Xie, Lisheng Liu, Jin Chen, Xiaorui Zhu, Wenyan Lv, Lingyun Ma, Wei Gao, Ziwen Hou, Jie She, Wandong Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress |
title | Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress |
title_full | Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress |
title_fullStr | Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress |
title_full_unstemmed | Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress |
title_short | Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress |
title_sort | glucocorticoids protect hei-oc1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8253451/ https://www.ncbi.nlm.nih.gov/pubmed/34250248 http://dx.doi.org/10.1515/biol-2021-0057 |
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