Detection of HSP 72 synthesis after acoustic overstimulation in rat cochlea

Lim, Ho Lim Hyun Ho; Jenkins, Oliver H.; Myers, Michael W.; Miller, Josef M.; Altschuler, Richard A.

doi:10.1016/0378-5955(93)90102-7

Cited by 82 publications

(5 citation statements)

References 30 publications

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“…HSPs are ubiquitously expressed in cells under physiological and pathological conditions, and their expression increases under stressful conditions, including noise exposure. When first induced by exposure to moderate sound levels, they can protect the ear from excessive noise exposure [47–50]. Three genes are responsible for HSPs synthesis: HSP70-1, HSP70-2 and HSP70-hom.…”

Section: Pathophysiology Of Nihlmentioning

confidence: 99%

Current insights in noise-induced hearing loss: a literature review of the underlying mechanism, pathophysiology, asymmetry, and management options

Le¹,

Straatman²,

Lea³

et al. 2017

J of Otolaryngol - Head & Neck Surg

302

235

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BackgroundNoise-induced hearing loss is one of the most common forms of sensorineural hearing loss, is a major health problem, is largely preventable and is probably more widespread than revealed by conventional pure tone threshold testing. Noise-induced damage to the cochlea is traditionally considered to be associated with symmetrical mild to moderate hearing loss with associated tinnitus; however, there is a significant number of patients with asymmetrical thresholds and, depending on the exposure, severe to profound hearing loss as well.Main bodyRecent epidemiology and animal studies have provided further insight into the pathophysiology, clinical findings, social and economic impacts of noise-induced hearing loss. Furthermore, it is recently shown that acoustic trauma is associated with vestibular dysfunction, with associated dizziness that is not always measurable with current techniques. Deliberation of the prevalence, treatment and prevention of noise-induced hearing loss is important and timely. Currently, prevention and protection are the first lines of defence, although promising protective effects are emerging from multiple different pharmaceutical agents, such as steroids, antioxidants and neurotrophins.ConclusionThis review provides a comprehensive update on the pathophysiology, investigations, prevalence of asymmetry, associated symptoms, and current strategies on the prevention and treatment of noise-induced hearing loss.

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Section: Pathophysiology Of Nihlmentioning

confidence: 99%

Current insights in noise-induced hearing loss: a literature review of the underlying mechanism, pathophysiology, asymmetry, and management options

Le¹,

Straatman²,

Lea³

et al. 2017

J of Otolaryngol - Head & Neck Surg

302

235

View full text Add to dashboard Cite

show abstract

“…In cochlea, HSF1 is constitutively expressed in hair cells, spiral ganglion cells and in the stria vascularis [4,5]. Expressional induction of Hsp70 occurs in the inner ear (cochlea) in response to hyperthermia [6], transient ischemia [7], acoustic overstimulation [8] and cisplatin [9]. The otoprotective role of HSPs in the cochlea is well documented.…”

Section: Introductionmentioning

confidence: 99%

Geldanamycin induces production of heat shock protein 70 and partially attenuates ototoxicity caused by gentamicin in the organ of Corti explants

Szczepek

Haupt

et al. 2009

J Biomed Sci

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BackgroundHeat shock protein 70 (HSP70) protects inner ear cells from damage and death induced by e.g. heat or toxins. Benzoquinone ansamycin antibiotic geldanamycin (GA) was demonstrated to induce the expression of HSP70 in various animal cell types. The aim of our study was to investigate whether GA induces HSP70 in the organ of Corti (OC), which contains the auditory sensory cells, and whether GA can protect these cells from toxicity caused by a common aminoglycoside antibiotic gentamicin.MethodsTo address these questions, we used the OC explants isolated from p3-p5 rats. As a read-out, we used RT-PCR, ELISA and immunofluorescence.ResultsWe found that GA at the concentration of 2 μM efficiently induced HSP70 expression on mRNA and protein level in the OC explants. Confocal microscopy revealed that HSP70 induced by GA is expressed by hair cells and interdental cells of spiral limbus. Preincubation of explants with 2 μM GA prior to adding gentamicin (500 μM) significantly reduced the loss of outer but not inner hair cells, suggesting different mechanisms of otoprotection needed for these two cell types.ConclusionGA induced HSP70 in the auditory sensory cells and partially protected them from toxicity of gentamicin. Understanding the molecular mechanisms of GA otoprotection may provide insights for preventative therapy of the hearing loss caused by aminoglycoside antibiotics.

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“…Therefore, in addition to mitochondrial damage, we conclude that ER stress is an important precursor of the intrinsic apoptosis pathway. Previous studies have induced HSP expression through exposure to various types of stress such as heat, acoustic trauma, and ischemia or ototoxicity of the inner ear [40]. HSP70 is a potent cytoprotective HSP that was recently shown to be protective against ototoxic hair cell degeneration when overexpressed in cochlear and vestibular tissues through transgenesis [41,42].…”

Section: Discussionmentioning

confidence: 99%

Heat Shock Factor 1 Prevents Age-Related Hearing Loss by Decreasing Endoplasmic Reticulum Stress

Lee

Gil

Jeong

et al. 2021

Cells

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Endoplasmic reticulum (ER) stress is a common stress factor during the aging process. Heat shock factor 1 (HSF1) plays a critical role in ER stress; however, its exact function in age-related hearing loss (ARHL) has not been fully elucidated. The purpose of the present study was to identify the role of HSF1 in ARHL. In this study, we demonstrated that the loss of inner and outer hair cells and their supporting cells was predominant in the high-frequency region (basal turn, 32 kHz) in ARHL cochleae. In the aging cochlea, levels of the ER stress marker proteins p-eIF2α and CHOP increased as HSF1 protein levels decreased. The levels of various heat shock proteins (HSPs) also decreased, including HSP70 and HSP40, which were markedly downregulated, and the expression levels of Bax and cleaved caspase-3 apoptosis-related proteins were increased. However, HSF1 overexpression showed significant hearing protection effects in the high-frequency region (basal turn, 32 kHz) by decreasing CHOP and cleaved caspase-3 and increasing the HSP40 and HSP70 proteins. These findings were confirmed by HSF1 functional studies using an auditory cell model. Therefore, we propose that HSF1 can function as a mediator to prevent ARHL by decreasing ER stress-dependent apoptosis in the aging cochlea.

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Detection of HSP 72 synthesis after acoustic overstimulation in rat cochlea

Cited by 82 publications

References 30 publications

Current insights in noise-induced hearing loss: a literature review of the underlying mechanism, pathophysiology, asymmetry, and management options

Current insights in noise-induced hearing loss: a literature review of the underlying mechanism, pathophysiology, asymmetry, and management options

Geldanamycin induces production of heat shock protein 70 and partially attenuates ototoxicity caused by gentamicin in the organ of Corti explants

Heat Shock Factor 1 Prevents Age-Related Hearing Loss by Decreasing Endoplasmic Reticulum Stress

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