Deficiency in plasma membrane calcium ATPase isoform 2 increases susceptibility to noise-induced hearing loss in mice

Kozel, Peter; Davis, Roger T.; Krieg, Edward F.; Shull, Gary E.; Erway, Lawrence C.

doi:10.1016/s0378-5955(01)00420-8

Cited by 78 publications

(63 citation statements)

References 33 publications

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“…The automatic motility of outer hair cells endows the cochlea with the function of feedback regulation, modulating the hair bundle deflection through the electromechanical transduction. As a main component of hair cell skeleton, F-actin provides a substantial base for motility of outer hair cells, and is thought to be concerned with the pathological changes of hair cells at the advanced stage 8,20,21) . CaM is a major intracellular calcium receptor found in many different cell types, which maintains intracellular calcium homeostasis, and as a result protects cytoskeleton from degradation.…”

Section: Discussionmentioning

confidence: 99%

Changes in Guinea Pig Cochlear Hair Cells after Sound Conditioning and Noise Exposure

Zuo¹,

Cui²,

She³

et al. 2008

Journal of Occupational Health

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Changes in Guinea Pig Cochlear Hair Cells after Sound Conditioning and NoiseExposure: Hongyan ZUO, et al. Department of Occupational Hygiene, Institute of Health and Environmental Medicine of Tianjin, PR ChinaSound conditioning has reduced noise-induced hearing loss in experimental mammalian animals and in clinical observation. Forty guinea pigs were grouped as: A, control; B, conditioning noise exposure group; C, high level noise exposure group; and D, conditioning noise exposure followed by a high level noise exposure group. Auditory brainstem response thresholds were measured. The cochlear sensory epithelia surface was observed microscopically. Calmodulin, F-actin and heat shock protein 70 (HSP70) in hair cells were immunohistochemistrically stained. The intracellular free calcium was stained for confocal microscopy. The ABR threshold shift after noise exposure was higher in group C than D, and showed a quicker and better recovery in group D than C. Stereocilia loss and the disarrangement of outer hair cells were observed, with the greatest changes seen in group C, followed by g r o u p s D a n d B .T h e m o s t i n t e n s i v e immunohistochemical intracellular expressions of calmodulin, F-actin, and HSP70 were found in group D, followed by groups C, B and A. The highest intensity of the fluorescent intracellular free Ca 2+ staining in the isolated outer hair cells was observed in group C. The ABR and morphological studies confirmed the protective effect from noise trauma of sound conditioning. The protective mechanism of hair cells during sound conditioning was enforced through the increase of cellular cytoskeleton proteins and through the relieving of intracellular calcium overloading caused by the traumatic noise. (J Occup Health 2008; 50: 373-379)

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Section: Discussionmentioning

confidence: 99%

Changes in Guinea Pig Cochlear Hair Cells after Sound Conditioning and Noise Exposure

Zuo¹,

Cui²,

She³

et al. 2008

Journal of Occupational Health

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“…Furthermore, studies of heterozygous deaf-waddler mice show that partial loss of Atp2b2 activity modifies, but is not itself sufficient to cause, HL, and haploinsufficiency at Atp2b2 and homozygosity of Cdh23 753A together, but neither alone, cause early-onset HL in mdfw mice (Atp2b2+/dfw-2J mdfw/mdfw). It has also been reported that heterozygosity for a null allele of Atp2b2 predisposes mice to noise-induced sensorineural hearing loss [47]. Reciprocally, in humans, a hypofunctional variant (V586M) in ATP2B2 has also been found associated with increased HL caused by a homozygous mutation in CDH23 in a manner analogous to the interaction between the dfw 2J allele of Atp2b2 and the ahl allele of Cdh23 in mice.…”

Section: Heritability Allelism and Genetic Modifiers Of Presbycusismentioning

confidence: 94%

Ageing and hearing loss

Yan

2007

The Journal of Pathology

278

178

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Although many adults retain good hearing as they age, hearing loss associated with ageing is common among elderly persons. There are a number of pathophysiolological processes underlying age-related changes to functional components in the inner ear. Genetic factors determine the ageing process but are under the influence of intrinsic and environmental factors. It is difficult to distinguish changes of normal ageing from those of other contributing factors. The effects of age-related deafness can have significant physical, functional and mental health consequences. Although a deficit in hearing can be corrected to some degree by a hearing aid or other appropriate amplification devices, hearing-related rehabilitative needs are much more than simply amplifying external sound. Only by better understanding the process of ageing and its effect on the auditory function can we better accommodate elderly people in our day-to-day interactions. We review here the structure and function of the inner ear, pathophysiology associated with age-related hearing loss (ARHL), heritability, allelism and modifier genes of ARHL, and evaluate the genetic analyses for identification of genetic factors that are involved.

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“…4 -8 Animal studies have confirmed the assumption that genetic factors influence the susceptibility to NIHL. 9 Knockout mice, such as Pmca2À/À, 10 Cdh23 þ /À, 11 Sod1À/À 12 and Gpx1À/À, 13 are more susceptible to noise than their wild-type littermates. Mouse strains with agerelated hearing impairment and spontaneously hypertensive rats are more sensitive to noise than other mouse strains and normotensive rats, respectively.…”

Section: Introductionmentioning

confidence: 99%

Variations in HSP70 genes associated with noise-induced hearing loss in two independent populations

et al. 2008

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Noise-induced hearing loss (NIHL) is one of the most important occupational health hazards. Millions of people worldwide are exposed daily to harmful levels of noise. NIHL is a complex disease resulting from an interaction between genetic and environmental factors. Although the environmental risk factors have been studied extensively, little is known about the genetic factors. Heat-shock proteins (HSPs) are induced after exposure to severe noise. When first induced by exposure to moderate sound levels, they can protect the ear from damage from excessive noise exposure. This protection is highly variable between individuals. An association of HSP70 genes with NIHL has been described by Yang et al (2006) in a Chinese sample set of noise-exposed workers. In this study, three polymorphisms (rs1043618, rs1061581 and rs2227956) in HSP70-1, HSP70-2 and HSP70-hom, respectively, were genotyped in 206 Swedish and 238 Polish DNA samples of noise-exposed subjects and analyzed. One SNP, rs2227956 in HSP70-hom, resulted in a significant association with NIHL in both sample sets. In addition, rs1043618 and rs1061581 were significant in the Swedish sample set. Analysis of the haplotypes composed of the three SNPs revealed significant associations between NIHL and haplotype GAC in both sample sets and with haplotype CGT in the Swedish sample set. In conclusion, this study replicated the association of HSP70 genes with NIHL in a second and third independent noise-exposed sample set, hereby adding to the evidence that HSP70 genes may be NIHL susceptibility genes.

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Deficiency in plasma membrane calcium ATPase isoform 2 increases susceptibility to noise-induced hearing loss in mice

Cited by 78 publications

References 33 publications

Changes in Guinea Pig Cochlear Hair Cells after Sound Conditioning and Noise Exposure

Changes in Guinea Pig Cochlear Hair Cells after Sound Conditioning and Noise Exposure

Ageing and hearing loss

Variations in HSP70 genes associated with noise-induced hearing loss in two independent populations

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