Over-expression of myosin7A in cochlear hair cells of circling mice

Kim, Yoo Yeon; Nam, Hajin; Jung, Harry; Kim, Boyoung; Suh, Jun-Gyo

doi:10.5625/lar.2017.33.1.1

Cited by 5 publications

(4 citation statements)

References 23 publications

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“…The specimens were incubated in 5% normal goat serum for 1 h at RT to prevent nonspecific labeling. Then, the specimens were incubated with the primary antibody, MYO7A (1:200, ab3481, Abcam, UK), for 1 h at 4 °C [ 44 , 45 , 46 ]. Thereafter, the specimens were washed with PBS three times for five min each time, followed by incubation with a secondary antibody, goat anti-rabbit IgG H&L (Alexa Fluor ® 488; 1:1000, ab150077, Abcam, UK), for 1 h at RT.…”

Section: Methodsmentioning

confidence: 99%

Induced Short-Term Hearing Loss due to Stimulation of Age-Related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection

Choi

Lee

et al. 2020

IJMS

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Age-related hearing loss (ARHL) is the most common sensory disorder among the elderly, associated with aging and auditory hair cell death due to oxidative-stress-induced mitochondrial dysfunction. Although transgenic mice and long-term aging induction cultures have been used to study ARHL, there are currently no ARHL animal models that can be stimulated by intermittent environmental changes. In this study, an ARHL animal model was established by inducing continuous oxidative stress to promote short-term aging of cells, determined on the basis of expression of hearing-loss-induced phenotypes and aging-related factors. The incidence of hearing loss was significantly higher in dual- and triple-exposure conditions than in intermittent hypoxic conditions, high-fat diet (HFD), or d-galactose injection alone. Continuous oxidative stress and HFD accelerated cellular aging. An increase in Ucp2, usually expressed during mitochondrial dysfunction, was observed. Expression of Cdh23, Slc26a4, Kcnq4, Myo7a, and Myo6, which are ARHL-related factors, were modified by oxidative stress in the cells of the hearing organ. We found that intermittent hypoxia, HFD, and galactose injection accelerated cellular aging in the short term. Thus, we anticipate that the development of this hearing loss animal model, which reflects the effects of intermittent environmental changes, will benefit future research on ARHL.

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Section: Methodsmentioning

confidence: 99%

Induced Short-Term Hearing Loss due to Stimulation of Age-Related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection

Choi

Lee

et al. 2020

IJMS

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“…Myosin7a is critical for the development and arrangement of hair bundles. 23 Cisplatin is known to induce a decrease in Myosin 7a + cell count in rats cochlear organotypic culture. 24 Based on the cochlear organotypic culture, HEI-OC1 cell culture, and CCK-8 detection of cell viability, we found that SFN protected hair cell count, increased Myosin 7a + cell count, prevented HEI-OC1 cell death, and increased cell viability in vitro.…”

Section: Discussionmentioning

confidence: 99%

Sulforaphane attenuates cisplatin-induced hearing loss by inhibiting histone deacetylase expression

Wang

Tian

Fang

et al. 2021

Int J Immunopathol Pharmacol

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Introduction Cruciferous vegetables are a rich source of sulforaphane (SFN), which acts as a natural HDAC inhibitor (HDACi). Our previous study found that HDACi could restore histone acetyltransferase/histone deacetylase (HAT/HDAC) balance in the cochlea and attenuate gentamicin-induced hearing loss in guinea pigs. Here, we investigated the protective effect of SFN on cisplatin-induced hearing loss (CIHL). Methods Thirty rats were randomly divided into 3 equal groups: the control group, cisplatin group, and SFN+cisplatin group. Rats were injected with SFN (30 mg/kg once a day) and cisplatin (7 mg/kg twice a day) for 7 days to investigate the protective role of SFN on CIHL. We observed auditory brainstem response (ABR) threshold shifts and immunostained cochlear basilar membranes of rats. For in vitro experiments, we treated HEI-OC1 cells and rat cochlear organotypic cultures with SFN (5, 10, and 15 μM) and cisplatin (10 μM). Immunofluorescence, cell viability, and protein analysis were performed to further analyze the protective mechanism of SFN on CIHL. Results SFN (30 mg/kg once a day) decreased cisplatin (7 mg/kg twice a day)-induced ABR threshold shifts and outer hair cell loss. CCK-8 assay showed that cisplatin (10 μM) reduced the viability of HEI-OC1 cells to 42%, and SFN had a dose-dependent protective effect. In cochlear organotypic cultures, we found that SFN (10 and 15 μM) increased cisplatin (10 μM)-induced myosin 7a+ cell count and restored ciliary morphology. SFN (5, 10, and 15 μM) reversed the cisplatin (10 μM)-induced increase in HDAC2, -4, and -5 and SFN (15 μM) reversed the cisplatin (10 μM)-induced decrease in H3-Ack9 [acetyl-histone H3 (Lys9)] protein expression in HEI-OC1 cells. Neither cisplatin nor cisplatin combined with SFN affected the expression of HDAC7, or HDAC9. Conclusion SFN prevented disruption of the HAT/HDAC balance, protecting against CIHL in rats.

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“…TMIE is likely to collaborate with the MYO7A in the development and maintenance of the stereociliary bundles during the postnatal developmental stages of the cochlea. The expression level of Myo7a increased by 3‐folds in cir/+ and cir/cir against the wild‐type mice at P5, suggesting that the overexpression of Myo7a can be a compensatory mechanism in order to fix the damaged stereocilia in the circling mice in the absence of the TMIE protein 58 …”

Section: Tmie Connects To Other Members In Mechanotransductionmentioning

confidence: 99%

How Transmembrane Inner Ear (TMIE) plays role in the auditory system: A mystery to us

Farhadi

Razmara

Balali

et al. 2021

J Cellular Molecular Medi

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Different cellular mechanisms contribute to the hearing sense, so it is obvious that any disruption in such processes leads to hearing impairment that greatly influences the global economy and quality of life of the patients and their relatives. In the past two decades, transmembrane inner ear (TMIE) protein has received a great deal of research interest because its impairments cause hereditary deafness in humans. This evolutionarily conserved membrane protein contributes to a fundamental complex that plays role in the maintenance and function of the sensory hair cells. Although the critical roles of the TMIE in mechanoelectrical transduction or hearing procedures have been discussed, there are little to no review papers summarizing the roles of the TMIE in the auditory system. In order to fill this gap, herein, we discuss the important roles of this protein in the auditory system including its role in mechanotransduction, olivocochlear synapse, morphology and different signalling pathways; we also review the genotype‐phenotype correlation that can per se show the possible roles of this protein in the auditory system.

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Over-expression of myosin7A in cochlear hair cells of circling mice

Cited by 5 publications

References 23 publications

Induced Short-Term Hearing Loss due to Stimulation of Age-Related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection

Induced Short-Term Hearing Loss due to Stimulation of Age-Related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection

Sulforaphane attenuates cisplatin-induced hearing loss by inhibiting histone deacetylase expression

How Transmembrane Inner Ear (TMIE) plays role in the auditory system: A mystery to us

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