ArticleOpen life sciences2021
Glucocorticoids protect HEI-OC1 cells from tunicamycin-induced cell damage via inhibiting endoplasmic reticulum stress.
Article in Open life sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- GRP78 protein metabolism in obese and diabetic rats: a study of its role in metabolic disorders.Diabetology & metabolic syndrome · 2024Article
- Potent carotenoid astaxanthin expands the anti-cancer activity of cisplatin in human prostate cancer cells.Journal of natural medicines · 2023Article
- Selenium Protects Mouse Hypothalamic Cells from Glucocorticoid-Induced Endoplasmic Reticulum Stress Vulnerability and Insulin Signaling Impairment.Antioxidants (Basel, Switzerland) · 2023Article
- Article
- Resveratrol Ameliorates Lipopolysaccharide-Induced Sudden Sensorineural Hearing Loss inEvidence-based complementary and alternative medicine : eCAM · 2022Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo 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.
methodsIn the present study, we established an
resultsIn 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.
conclusionDexamethasone 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.
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