Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress
Related Experiment Video
Updated: Oct 29, 2025
Working with Auditory HEI-OC1 Cells
Published on: September 3, 2016
Zhibiao Liu1,2, Bing Fei3, Lisheng Xie1
1Department of Otolaryngology-Head and Neck Surgery, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, 321 Zhongshan Road, Nanjing 210008, China.
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.
Insights
Glucocorticoids like dexamethasone protect against endoplasmic reticulum stress (ERS) in hearing loss models. This study shows dexamethasone reduces ERS markers in hair cells, suggesting a therapeutic mechanism for sensorineural hearing loss.
Area of Science:
- Oto-neuroscience
- Cellular Biology
- Pharmacology
Background:
- Sensorineural hearing loss (SNHL) is often linked to endoplasmic reticulum stress (ERS).
- The protein kinase RNA-like ER kinase (PERK)-C/EBP homologous protein (CHOP) pathway is a key mediator of ERS.
- Understanding glucocorticoid (GC) mechanisms in ERS is crucial for SNHL treatment.
Purpose of the Study:
- To investigate the role of the PERK-CHOP pathway in dexamethasone's protective effects against ERS.
- To analyze how GCs influence ERS in a hair cell model relevant to SNHL.
Main Methods:
- An in vitro ERS model was created using HEI-OC1 cells treated with tunicamycin.
- Dexamethasone's effects on cell proliferation, apoptosis, and the ATF4-CHOP pathway were assessed.
- Techniques included CCK-8 assay, flow cytometry, western blotting, and RT-PCR.
Main Results:
- Dexamethasone significantly reduced tunicamycin-induced ATF4 and CHOP expression in HEI-OC1 cells.
- Cell viability and proliferation were maintained despite ERS induction.
- The protective effect of dexamethasone was reversed by a glucocorticoid antagonist.
Conclusions:
- Dexamethasone demonstrates a protective effect on hair-cell-like cells against ERS-induced damage.
- This finding suggests a potential mechanism for glucocorticoid treatment in SNHL.
- Targeting the PERK-CHOP pathway may be a therapeutic strategy for SNHL.
More Related Videos
09:57In Vitro Assays to Evaluate the Migration, Invasion, and Proliferation of Immortalized Human First-trimester Trophoblast Cell Lines
Published on: March 5, 2019
09:22The Cell-based L-Glutathione Protection Assays to Study Endocytosis and Recycling of Plasma Membrane Proteins
Published on: December 13, 2013
