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Hearing Disorders: HELP
Articles by Shinichi Someya
Based on 10 articles published since 2009
(Why 10 articles?)
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Between 2009 and 2019, Shinichi Someya wrote the following 10 articles about Hearing Disorders.
 
+ Citations + Abstracts
1 Review Maintaining good hearing: calorie restriction, Sirt3, and glutathione. 2013

Han, Chul / Someya, Shinichi. ·Department of Aging and Geriatric Research, University of Florida, Gainesville, FL 32610, USA. ·Exp Gerontol · Pubmed #23454634.

ABSTRACT: Reducing calorie intake extends the lifespan of a variety of experimental models and delays progression of age-related hearing loss (AHL). AHL is a common feature of aging and is characterized by age-related decline of hearing associated with loss of sensory hair cells, spiral ganglion neurons, and/or stria vascularis degeneration in the cochlea. Sirtuins are a family of NAD(+)-dependent enzymes that regulate lifespan in lower organisms and have emerged as broad regulators of cellular fate. Our recent study indicated that mitochondrial Sirt3, a member of the sirtuin family, mediates the anti-aging effects of calorie restriction (CR) on AHL in mice. Interestingly, we also found that weight loss alone may not be sufficient for maintaining normal hearing. How does CR slow the progression of AHL through regulation of Sirt3? Here we review the evidence that during CR, Sirt3 slows the progression of AHL by promoting the glutathione-mediated mitochondrial antioxidant defense system in mice. A significant reduction in food consumption in one's daily life may not be a desirable and realistic option for most people. Therefore, identification/discovery of compounds that induce the activation of SIRT3 or glutathione reductase, or that increase mitochondrial glutathione levels has potential for maintaining good hearing through mimicking the anti-aging effects of CR in human inner ear cells.

2 Review Current concepts in age-related hearing loss: epidemiology and mechanistic pathways. 2013

Yamasoba, Tatsuya / Lin, Frank R / Someya, Shinichi / Kashio, Akinori / Sakamoto, Takashi / Kondo, Kenji. ·Department of Otolaryngology and Head and Neck Surgery, University of Tokyo, Tokyo, Japan. tyamasoba-tky@umin.ac.jp ·Hear Res · Pubmed #23422312.

ABSTRACT: Age-related hearing loss (AHL), also known as presbycusis, is a universal feature of mammalian aging and is characterized by a decline of auditory function, such as increased hearing thresholds and poor frequency resolution. The primary pathology of AHL includes the hair cells, stria vascularis, and afferent spiral ganglion neurons as well as the central auditory pathways. A growing body of evidence in animal studies has suggested that cumulative effect of oxidative stress could induce damage to macromolecules such as mitochondrial DNA (mtDNA) and that the resulting accumulation of mtDNA mutations/deletions and decline of mitochondrial function play an important role in inducing apoptosis of the cochlear cells, thereby the development of AHL. Epidemiological studies have demonstrated four categories of risk factors of AHL in humans: cochlear aging, environment such as noise exposure, genetic predisposition, and health co-morbidities such as cigarette smoking and atherosclerosis. Genetic investigation has identified several putative associating genes, including those related to antioxidant defense and atherosclerosis. Exposure to noise is known to induce excess generation of reactive oxygen species (ROS) in the cochlea, and cumulative oxidative stress can be enhanced by relatively hypoxic situations resulting from the impaired homeostasis of cochlear blood supply due to atherosclerosis, which could be accelerated by genetic and co-morbidity factors. Antioxidant defense system may also be influenced by genetic backgrounds. These may explain the large variations of the onset and extent of AHL among elderly subjects. This article is part of a Special Issue entitled "Annual Reviews 2013".

3 Review Mouse models of age-related mitochondrial neurosensory hearing loss. 2013

Han, Chul / Someya, Shinichi. ·Department of Aging, Division of Biology of Aging, University of Florida, 1600 SW Archer Road, PO Box 100143, Gainesville, FL 32610-0143, USA. ·Mol Cell Neurosci · Pubmed #22820179.

ABSTRACT: Hearing loss is the most common sensory disorder in the elderly population. Overall, 10% of the population has a hearing loss in the US, and this age-related hearing disorder is projected to afflict more than 28 million Americans by 2030. Age-related hearing loss is associated with loss of sensory hair cells (sensory hearing loss) and/or spiral ganglion neurons (neuronal hearing loss) in the cochlea of the inner ear. Many lines of evidence indicate that oxidative stress and associated mitochondrial dysfunction play a central role in age-related neurodegenerative diseases and are a cause of age-related neurosensory hearing loss. Yet, the molecular mechanisms of how oxidative stress and/or mitochondrial dysfunction lead to hearing loss during aging remain unclear, and currently there is no treatment for this age-dependent disorder. Several mouse models of aging and age-related diseases have been linked to age-related mitochondrial neurosensory hearing loss. Evaluation of these animal models has offered basic knowledge of the mechanism underlying hearing loss associated with oxidative stress, mitochondrial dysfunction, and aging. Here we review the evidence that specific mutations in the mitochondrial DNA or nuclear DNA that affect mitochondrial function result in increased oxidative damage and associated loss of sensory hair cells and/or spiral ganglion neurons in the cochlea during aging, thereby causing hearing loss in these mouse models. Future studies comparing these models will provide further insight into fundamental knowledge about the disordered process of hearing and treatments to improve the lives of individuals with communication disorders. This article is part of a Special Issue entitled 'Mitochondrial function and dysfunction in neurodegeneration'.

4 Review Mitochondrial oxidative damage and apoptosis in age-related hearing loss. 2010

Someya, Shinichi / Prolla, Tomas A. ·Department of Genetics, University of Wisconsin, Madison, WI 53706, USA. ·Mech Ageing Dev · Pubmed #20434479.

ABSTRACT: Age-related hearing loss (AHL) is a universal feature of mammalian aging and is the most common sensory disorder in the elderly population. Experimental evidence suggests that mitochondrial dysfunction associated with reactive oxygen species (ROS) plays a central role in the aging process of cochlear cells. Although it is well established that mitochondria are the major source of ROS in the cell, specific molecular mechanisms of aging induced by ROS remain poorly characterized. Here we review the evidence that supports a central role for Bak-mediated mitochondrial apoptosis in AHL. We also propose that this mechanism may be of general relevance to age-related cell death in long-lived post-mitotic cells of multiple tissues, providing an opportunity for a targeted therapeutic intervention in human aging.

5 Review Effects of caloric restriction on age-related hearing loss in rodents and rhesus monkeys. 2010

Someya, Shinichi / Tanokura, Masaru / Weindruch, Richard / Prolla, Tomas A / Yamasoba, Tatsuya. ·Departments of Genetics & Medical Genetics, University of Wisconsin, Madison, WI 53706, USA. ·Curr Aging Sci · Pubmed #20298166.

ABSTRACT: Age-related hearing loss (AHL), also known as presbycusis, is a universal feature of mammalian aging and is the most frequently occurring sensory disorder in the elderly population. AHL is characterized by a decline of auditory function and loss of hair cells and spiral ganglion neurons in the cochlea of the inner ear. It has been postulated that AHL occurs gradually as a result of the cumulative effect with aging of exposure to noise, diet, oxidative damage, and mitochondrial DNA mutations. However, the molecular mechanisms of AHL remain unclear and no preventative or therapeutic interventions have been developed. A growing body of evidence suggests increased oxidative damage with aging to macromolecules such as DNA, proteins, and lipids may play a causal role in aging and age-related diseases. Caloric restriction (CR) extends the lifespan of most mammalian species, delays the onset of multiple age-related diseases, and attenuates both the degree of oxidative damage and the associated decline in physiological function. Here, we review studies on CR's ability to prevent cochlear pathology and AHL in laboratory animals and discuss potential molecular mechanisms of CR's actions.

6 Article Loss of sestrin 2 potentiates the early onset of age-related sensory cell degeneration in the cochlea. 2017

Zhang, Celia / Sun, Wei / Li, Ji / Xiong, Binbin / Frye, Mitchell D / Ding, Dalian / Salvi, Richard / Kim, Mi-Jung / Someya, Shinichi / Hu, Bo Hua. ·Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, 137 Cary Hall, Buffalo, NY 14214, USA. Electronic address: celiazha@buffalo.edu. · Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, 137 Cary Hall, Buffalo, NY 14214, USA. Electronic address: weisun@buffalo.edu. · University of Mississippi Medical Center, Department of Physiology and Biophysics, University of Mississippi, 2500 North State Street, Jackson, MS 39216, USA. Electronic address: jli3@umc.edu. · Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, 137 Cary Hall, Buffalo, NY 14214, USA. Electronic address: xiongbb2015@126.com. · Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, 137 Cary Hall, Buffalo, NY 14214, USA. Electronic address: mfrye@buffalo.edu. · Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, 137 Cary Hall, Buffalo, NY 14214, USA. Electronic address: dding@buffalo.edu. · Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, 137 Cary Hall, Buffalo, NY 14214, USA. Electronic address: salvi@buffalo.edu. · Departments of Aging and Geriatric Research, College of Medicine, University of Florida, 1600 SW Archer Road, Gainesville, FL 32610, USA. Electronic address: mijungkim@ufl.edu. · Departments of Aging and Geriatric Research, College of Medicine, University of Florida, 1600 SW Archer Road, Gainesville, FL 32610, USA. Electronic address: someya@ufl.edu. · Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, 137 Cary Hall, Buffalo, NY 14214, USA. Electronic address: bhu@buffalo.edu. ·Neuroscience · Pubmed #28818524.

ABSTRACT: Sestrin 2 (SESN2) is a stress-inducible protein that protects tissues from oxidative stress and delays the aging process. However, its role in maintaining the functional and structural integrity of the cochlea is largely unknown. Here, we report the expression of SESN2 protein in the sensory epithelium, particularly in hair cells. Using C57BL/6J mice, a mouse model of age-related cochlear degeneration, we observed a significant age-related reduction in SESN2 expression in cochlear tissues that was associated with early onset hearing loss and accelerated age-related sensory cell degeneration that progressed from the base toward the apex of the cochlea. Hair cell death occurred by caspase-8 mediated apoptosis. Compared to C57BL/6J control mice, Sesn2 KO mice displayed enhanced expression of proinflammatory genes and activation of basilar membrane macrophages, suggesting that loss of SESN2 function provokes the immune response. Together, these results suggest that Sesn2 plays an important role in cochlear homeostasis and immune responses to stress.

7 Article Effects of Long-Term Exercise on Age-Related Hearing Loss in Mice. 2016

Han, Chul / Ding, Dalian / Lopez, Maria-Cecilia / Manohar, Senthilvelan / Zhang, Yanping / Kim, Mi-Jung / Park, Hyo-Jin / White, Karessa / Kim, Yong Hwan / Linser, Paul / Tanokura, Masaru / Leeuwenburgh, Christiaan / Baker, Henry V / Salvi, Richard J / Someya, Shinichi. ·Department of Aging and Geriatric Research. · Center for Hearing and Deafness, State University of New York at Buffalo, Buffalo, New York 14214, and. · Department of Molecular Genetics and Microbiology. · Gene Expression and Genotyping, Interdisciplinary Center for Biotechnology Research, and. · Whitney Laboratory, University of Florida, St. Augustine, Florida 32080. · Department of Physiology and Functional Genomics, University of Florida, Gainesville, Florida 32610. · Department of Applied Biological Chemistry, University of Tokyo, Yayoi, Tokyo, 113, Japan. · Department of Aging and Geriatric Research, someya@ufl.edu. ·J Neurosci · Pubmed #27807171.

ABSTRACT: Regular physical exercise reduces the risk for obesity, cardiovascular diseases, and disability and is associated with longer lifespan expectancy (Taylor et al., 2004; Pahor et al., 2014; Anton et al., 2015; Arem et al., 2015). In contrast, decreased physical function is associated with hearing loss among older adults (Li et al., 2013; Chen et al., 2015). Here, we investigated the effects of long-term voluntary wheel running (WR) on age-related hearing loss (AHL) in CBA/CaJ mice, a well established model of AHL (Zheng et al., 1999). WR activity peaked at 6 months of age (12,280 m/d) and gradually decreased over time. At 24 months of age, the average WR distance was 3987 m/d. Twenty-four-month-old runners had less cochlear hair cell and spiral ganglion neuron loss and better auditory brainstem response thresholds at the low and middle frequencies compared with age-matched, non-WR controls. Gene ontology (GO) enrichment analysis of inner ear tissues from 6-month-old controls and runners revealed that WR resulted in a marked enrichment for GO gene sets associated with immune response, inflammatory response, vascular function, and apoptosis. In agreement with these results, there was reduced stria vascularis (SV) atrophy and reduced loss of capillaries in the SV of old runners versus old controls. Given that SV holds numerous capillaries that are essential for transporting oxygen and nutrients into the cochlea, our findings suggest that long-term exercise delays the progression of AHL by reducing age-related loss of strial capillaries associated with inflammation. SIGNIFICANCE STATEMENT: Nearly two-thirds of adults aged 70 years or older develop significant age-related hearing loss (AHL), a condition that can lead to social isolation and major communication difficulties. AHL is also associated with decreased physical function among older adults. In the current study, we show that regular exercise slowed AHL and cochlear degeneration significantly in a well established murine model. Our data suggest that regular exercise delays the progression of AHL by reducing age-related loss of strial capillaries associated with inflammation.

8 Article Sirt1 deficiency protects cochlear cells and delays the early onset of age-related hearing loss in C57BL/6 mice. 2016

Han, Chul / Linser, Paul / Park, Hyo-Jin / Kim, Mi-Jung / White, Karessa / Vann, James M / Ding, Dalian / Prolla, Tomas A / Someya, Shinichi. ·Department of Aging and Geriatric Research, University of Florida, Gainesville, FL, USA. · Whitney Laboratory, University of Florida, St Augustine, FL, USA. · Department of Neurology, University of Florida, Gainesville, FL, USA. · Department of Genetics, University of Wisconsin, Madison, WI, USA; Department of Medical Genetics, University of Wisconsin, Madison, WI, USA. · Center for Hearing and Deafness, State University of New York at Buffalo, NY, USA. · Department of Aging and Geriatric Research, University of Florida, Gainesville, FL, USA. Electronic address: someya@ufl.edu. ·Neurobiol Aging · Pubmed #27255815.

ABSTRACT: Hearing gradually declines with age in both animals and humans, and this condition is known as age-related hearing loss (AHL). Here, we investigated the effects of deficiency of Sirt1, a member of the mammalian sirtuin family, on age-related cochlear pathology and associated hearing loss in C57BL/6 mice, a mouse model of early-onset AHL. Sirt1 deficiency reduced age-related oxidative damage of cochlear hair cells and spiral ganglion neurons and delayed the early onset of AHL. In cultured mouse inner ear cell lines, Sirt1 knockdown increased cell viability under oxidative stress conditions, induced nuclear translocation of Foxo3a, and increased acetylation status of Foxo3a. This resulted in increased activity of the antioxidant enzyme catalase. In young wild-type mice, both Sirt1 and Foxo3a proteins resided in the cytoplasm of the supporting cells within the organ of Corti of the cochlea. Therefore, our findings suggest that SIRT1 promotes early-onset AHL through suppressing FOXO3a-mediated oxidative stress resistance in the cochlea of C57BL/6 mice.

9 Article Sirt3 mediates reduction of oxidative damage and prevention of age-related hearing loss under caloric restriction. 2010

Someya, Shinichi / Yu, Wei / Hallows, William C / Xu, Jinze / Vann, James M / Leeuwenburgh, Christiaan / Tanokura, Masaru / Denu, John M / Prolla, Tomas A. ·Departments of Genetics and Medical Genetics, University of Wisconsin, Madison, 53706, USA. ·Cell · Pubmed #21094524.

ABSTRACT: Caloric restriction (CR) extends the life span and health span of a variety of species and slows the progression of age-related hearing loss (AHL), a common age-related disorder associated with oxidative stress. Here, we report that CR reduces oxidative DNA damage in multiple tissues and prevents AHL in wild-type mice but fails to modify these phenotypes in mice lacking the mitochondrial deacetylase Sirt3, a member of the sirtuin family. In response to CR, Sirt3 directly deacetylates and activates mitochondrial isocitrate dehydrogenase 2 (Idh2), leading to increased NADPH levels and an increased ratio of reduced-to-oxidized glutathione in mitochondria. In cultured cells, overexpression of Sirt3 and/or Idh2 increases NADPH levels and protects from oxidative stress-induced cell death. Therefore, our findings identify Sirt3 as an essential player in enhancing the mitochondrial glutathione antioxidant defense system during CR and suggest that Sirt3-dependent mitochondrial adaptations may be a central mechanism of aging retardation in mammals.

10 Article Age-related hearing loss in C57BL/6J mice is mediated by Bak-dependent mitochondrial apoptosis. 2009

Someya, Shinichi / Xu, Jinze / Kondo, Kenji / Ding, Dalian / Salvi, Richard J / Yamasoba, Tatsuya / Rabinovitch, Peter S / Weindruch, Richard / Leeuwenburgh, Christiaan / Tanokura, Masaru / Prolla, Tomas A. ·Department of Genetics and Medical Genetics, Veterans Administration Hospital, Geriatric Research Education and Clinical Center, University of Wisconsin, Madison, WI 53706, USA. ·Proc Natl Acad Sci U S A · Pubmed #19901338.

ABSTRACT: Age-related hearing loss (AHL), known as presbycusis, is a universal feature of mammalian aging and is the most common sensory disorder in the elderly population. The molecular mechanisms underlying AHL are unknown, and currently there is no treatment for the disorder. Here we report that C57BL/6J mice with a deletion of the mitochondrial pro-apoptotic gene Bak exhibit reduced age-related apoptotic cell death of spiral ganglion neurons and hair cells in the cochlea, and prevention of AHL. Oxidative stress induces Bak expression in primary cochlear cells, and Bak deficiency prevents apoptotic cell death. Furthermore, a mitochondrially targeted catalase transgene suppresses Bak expression in the cochlea, reduces cochlear cell death, and prevents AHL. Oral supplementation with the mitochondrial antioxidants alpha-lipoic acid and coenzyme Q(10) also suppresses Bak expression in the cochlea, reduces cochlear cell death, and prevents AHL. Thus, induction of a Bak-dependent mitochondrial apoptosis program in response to oxidative stress is a key mechanism of AHL in C57BL/6J mice.