Related Experiment Video

Updated: Dec 6, 2025

Neuro-rehabilitation Approach for Sudden Sensorineural Hearing Loss

Neuro-rehabilitation Approach for Sudden Sensorineural Hearing Loss

Published on: January 25, 2016

GRβ Regulates Glucocorticoid Resistance in Sudden Sensorineural Hearing Loss

Xubo Chen¹, Qi Zhang², Chunping Yang¹

¹Department of Otolaryngology, Head and Neck Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, 330006, China.

Current Pharmaceutical Biotechnology

|October 9, 2020

Abstract

Background:

In recent years, the incidence of sudden deafness has gradually increased, with a very limited understanding of its etiology and pathogenesis. Glucocorticoids are the first choice of the treatment, but some hormone-resistant patients are not sensitive to glucocorticoid therapy. The pathogenesis is not yet known. In this study, we aim to construct the HEI-OC1 cell line stably overexpressing Glucocorticoid Receptor Beta (GRβ), and identify its exact role in the cases of glucocorticoidresistant sudden deafness.

Methods:

We used the endotoxin lipopolysaccharide-stimulated cochlear hair cells (HEI-OC1) to investigate the relationship of inflammation factor IL-2, TNF alpha, and SRp30c with the high expression GRβ. We built a stable GRβ high expression HEI-OC1 cell line and clarified its effects on the therapeutic effect of dexamethasone. MTT assay, colony formation assay, CCK-8 assay, Western blot, and RT-qPCR were utilized for characterizations.

Results:

Dexamethasone reduced the LPS-induced inflammatory response from HEI-OC1 cells (p<0.05), detected by MTT assay. Dexamethasone could protect HEI-OC1 cells, but its protective effect was weakened due to the transfection of SRp30c over-expression plasmid (p<0.05). The transfection of SRp30c over-expression plasmid in HEI-OC1 cells could elevate the expressions of GRβ (p<0.05).

Conclusion:

We clarified the mechanisms of high expression of GRβ in glucocorticoid-resistant sudden sensorineural hearing loss, and proved that the inhibition of SRp30c may act as a new treatment way of glucocorticoid-resistant sudden sensorineural hearing loss.

Insights

Sudden deafness is rising, and glucocorticoid resistance is a challenge. This study reveals that inhibiting SRp30c may offer a new treatment for glucocorticoid-resistant sudden sensorineural hearing loss by targeting GRβ expression.

Area of Science:

Otolaryngology
Molecular Biology
Pharmacology

Background:

Sudden deafness incidence is increasing, with poorly understood causes and limited treatment options for glucocorticoid-resistant cases.
Glucocorticoids are the primary treatment, but some patients do not respond, necessitating research into alternative therapeutic strategies.
The role of Glucocorticoid Receptor Beta (GRβ) in glucocorticoid resistance in sudden deafness is not yet fully elucidated.

Purpose of the Study:

To construct a HEI-OC1 cell line with stable overexpression of Glucocorticoid Receptor Beta (GRβ).
To investigate the role of GRβ in glucocorticoid-resistant sudden sensorineural hearing loss.
To explore the relationship between inflammation factors (IL-2, TNF alpha, SRp30c) and GRβ expression in cochlear hair cells.

Main Methods:

Utilized lipopolysaccharide-stimulated cochlear hair cells (HEI-OC1) to model inflammation.
Established a stable GRβ high expression HEI-OC1 cell line for experimental analysis.
Employed MTT assay, colony formation assay, CCK-8 assay, Western blot, and RT-qPCR to characterize cellular responses and gene expression.

Main Results:

Dexamethasone treatment reduced lipopolysaccharide-induced inflammation in HEI-OC1 cells (p<0.05).
Overexpression of SRp30c attenuated the protective effects of dexamethasone on HEI-OC1 cells (p<0.05).
SRp30c overexpression in HEI-OC1 cells led to elevated GRβ expression (p<0.05).

Conclusions:

Elucidated the mechanisms underlying high GRβ expression in glucocorticoid-resistant sudden sensorineural hearing loss.
Demonstrated that SRp30c plays a role in glucocorticoid resistance.
Identified SRp30c inhibition as a potential novel therapeutic strategy for glucocorticoid-resistant sudden sensorineural hearing loss.

Read full analysis

Keywords:

GRβ Glucocorticoid resistance LPS SRp30c dexamethasone sudden sensorineural hearing loss

More Related Videos

A Surgical Procedure for the Administration of Drugs to the Inner Ear in a Non-Human Primate Common Marmoset Callithrix jacchus

A Surgical Procedure for the Administration of Drugs to the Inner Ear in a Non-Human Primate Common Marmoset Callithrix jacchus

Published on: February 27, 2018

Cochlear Surface Preparation in the Adult Mouse

Cochlear Surface Preparation in the Adult Mouse

Published on: November 6, 2019

Related Concept Videos

GPCR Desensitization

GPCR Desensitization

G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...

Desensitization and Tachyphylaxis

Desensitization and Tachyphylaxis

Tachyphylaxis is described as a rapid decrease in response to a drug after repeated or continuous administration of the same drug dose. It is a phenomenon where the body becomes less responsive to a particular substance or intervention over time, requiring higher doses or stronger interventions to achieve the same effect. It results from adaptive changes in the body's receptors, signaling pathways, or physiological processes that occur in response to prolonged exposure to a stimulus.

Receptor Downregulation in MVBs

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...

GPCRs Regulate Adenylyl Cylase Activity

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...

G Protein-coupled Receptors

G Protein-coupled Receptors

G Protein-Coupled Receptors or GPCRs are membrane-bound receptors that transiently associate with heterotrimeric G proteins and induce an appropriate response to sensory stimuli such as light, odors, hormones, cytokines, or neurotransmitters.
GPCRs are also called heptahelical, 7TM, or serpentine receptors, and consist of seven (H1-H7) transmembrane alpha-helices that span the bilayer to form a cylindrical core. The transmembrane helices are connected by three extracellular loops and three...

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...

Articles linked to this work by shared authors, journal, and citation graph.

Integrative single-cell sequencing and machine learning analyses identify chronic inflammation and cancer-associated fibroblast subsets as drivers of adverse outcomes in ovarian cancer.

Translational oncology·2026

Mothers against decapentaplegic homolog 3-activated FAT atypical cadherin 2 regulates programmed death ligand-1 to mediate immune evasion in lung squamous cell carcinoma.

Mutation research·2026

Screening and Synergistic Effects of Phenoloxidase Inhibitors in Spodoptera litura.

Journal of agricultural and food chemistry·2026

DNAJB9 promotes epithelial-mesenchymal transition in the nasal epithelium of chronic rhinosinusitis by enhancing TRIM22-mediated IκBα degradation.

iScience·2026

Valorization of Rosa roxburghii Tratt pomace into green fluorescent carbon dots for functional reinforcement of polyvinyl alcohol-based active packaging films.

RSC advances·2026

An integrated clinical and imaging-based machine learning model to determine the preoperative nature of primary operable parotid tumors.

BMC oral health·2026

See all related articles