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Updated: Mar 6, 2026
Cochlear Implant Surgery and Electrically-evoked Auditory Brainstem Response Recordings in C57BL/6 Mice
Published on: January 9, 2019
Cochlear Transcriptome Following Acoustic Trauma and Dexamethasone Administration Identified by a Combination of
Yukihide Maeda1, Ryotaro Omichi, Akiko Sugaya
1Department of Otolaryngology-Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Kita-Ku, Okayama, Japan.
Aim:
To elucidate molecular mechanisms of noise-induced hearing loss (NIHL) and glucocorticoid therapy in the cochlea.
Background:
Glucocorticoids are used to treat many forms of acute sensorineural hearing loss, but their molecular action in the cochlea remains poorly understood.
Methods:
Dexamethasone was administered intraperitoneally immediately following acoustic overstimulation at 120 dB SPL for 2 hours to mice. The whole cochlear transcriptome was analyzed 12 and 24 hours following noise trauma and dexamethasone administration by both next-generation sequencing (RNA-seq) and DNA microarray. Differentially expressed genes (DEGs) with more than 2-fold changes after noise trauma and dexamethasone administration were identified. The functions of these DEGs were analyzed by David Bioinformatics Resources and a literature search.
Results:
Twelve hours after acoustic overstimulation, immune-related gene pathways such as "chemokine signaling activity," "cytokine-cytokine receptor interaction," and "cell adhesion molecules (CAMs) in the immune system" were significantly changed compared with the baseline level without noise. These DEGs were involved in immune and defense responses in the cochlea. Dexamethasone was administered to this NIHL model, and it modulated gene pathways of "cytokine-cytokine receptor interaction" and "cell adhesion molecules (CAMs) in the immune system" at 12 hours, compared with saline-injected control. Dexamethasone-dependent DEGs were also involved in immune and defense responses. A literature search showed that 10 other genes associated with hearing functions were regulated by dexamethasone both at 12 and 24 hours post-administration.
Conclusion:
Dexamethasone modulates the immune reaction in the traumatized cochlea following acoustic overstimulation. Dexamethasone may also regulate cochlear functions other than immunity.
Insights
Dexamethasone treatment modulates the immune response in the cochlea after noise-induced hearing loss. This study reveals how glucocorticoids affect gene expression in the damaged ear.
Area of Science:
- Oto-genetics and molecular biology
- Immunology and molecular mechanisms of hearing loss
Background:
- Glucocorticoids are clinically used for acute sensorineural hearing loss.
- The precise molecular mechanisms of glucocorticoid action in the cochlea are not well understood.
Purpose of the Study:
- To investigate the molecular mechanisms underlying noise-induced hearing loss (NIHL).
- To elucidate the effects of glucocorticoid therapy on the cochlea.
Main Methods:
- Mice were exposed to acoustic overstimulation and treated with dexamethasone.
- Whole cochlear transcriptomes were analyzed using RNA-seq and DNA microarray.
- Differentially expressed genes (DEGs) were identified and functionally analyzed.
Main Results:
- Noise trauma significantly altered immune-related gene pathways, including chemokine signaling and cytokine-cytokine receptor interactions.
- Dexamethasone modulated these immune pathways in the traumatized cochlea.
- Dexamethasone also regulated 10 other hearing-associated genes.
Conclusions:
- Dexamethasone influences the cochlear immune response following acoustic trauma.
- Glucocorticoids may have broader regulatory roles in cochlear function beyond immunity.
