Attenuation of hearing loss in DBA/2J mice by anti-apoptotic treatment

Yang, Linlin; Zhang, Heng; Xu, Han; Zhao, Xin; Hu, Fangyuan; Li, Ping; Xie, Gang; Gao, Lixiang; Cheng, Lin; Song, Xicheng; Han, Fengchan

doi:10.1016/j.heares.2015.05.006

Cited by 17 publications

(20 citation statements)

References 35 publications

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“…Apoptosis may play a potential role in the early onset of hearing loss (Yang et al, ). Gene expression profiles in the inner ears of DBA/2J mice at 5, 7, and 9 weeks of age were detected simultaneously in the mNGF‐treated and vehicle groups.…”

Section: Resultsmentioning

confidence: 99%

Otoprotective effects of mouse nerve growth factor in DBA/2J mice with early‐onset progressive hearing loss

Wang

Zhao

Zheng

et al. 2017

J of Neuroscience Research

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DBA/2J is an inbred mouse strain widely used in hearing research, as it displays progressive hair cell loss and degeneration of spiral ganglion neurons (SGNs) characterized by early-onset progressive hearing loss (ePHL). Mouse nerve growth factor (mNGF), as a common exogenous nerve growth factor (NGF), has been studied extensively for its ability to promote neuronal survival and growth. To determine whether mNGF can ameliorate progressive hearing loss (PHL) in DBA/2J mice, saline or mNGF was given to DBA/2J mice of either sex by daily intramuscular injection from the 1st to the 9th week after birth. At 5, 7, and 9 weeks of age, in comparison with vehicle groups, mNGF groups experienced decreased auditory-evoked brainstem response (ABR) thresholds and increased distortion product otoacoustic emission (DPOAE) amplitudes, the prevention of hair cell loss, and the inhibition of apoptosis of SGNs. Downregulation of Bak/Bax and Caspase genes and proteins in cochleae of mice receiving the mNGF treatment was detected by Real-time PCR, Western Blot and Immunohistochemistry. This suggests that the Bak-dependent mitochondrial apoptosis pathway may be involved in the otoprotective mechanism of mNGF in progressive hearing loss of DBA/2J mice. Our results demonstrate that mNGF can act as an otoprotectant in the DBA/2J mice for the early intervention of PHL and, thus, could become of great value in clinical applications.

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Section: Resultsmentioning

confidence: 99%

Otoprotective effects of mouse nerve growth factor in DBA/2J mice with early‐onset progressive hearing loss

Wang

Zhao

Zheng

et al. 2017

J of Neuroscience Research

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“…A number of specific and broad-spectrum peptide caspase inhibitors have been developed to elucidate the role of each specific caspase in cell death. Intraperitoneal injection of the pan-caspase-inhibitor z-VAD-FMK Z-VAD-FMK for eight weeks, starting at one week of age in DBA/2J and A/J mice, preserved hearing by more than 10 dB SPL in the ABR thresholds and significantly reduced OHC loss in the basal turns of the cochleae [120,121]. Even many caspase inhibitors (e.g., inhibitors of caspase-1, capses-2, caspase-6, and caspase-3) have been patented for their use in the treatments of neurodegenerative diseases, cardiovascular diseases, liver diseases, and cerebral stroke.…”

Section: Caspase Inhibitorsmentioning

confidence: 99%

Presbycusis: An Update on Cochlear Mechanisms and Therapies

Wang

Puel

2020

JCM

144

125

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Age-related hearing impairment (ARHI), also referred to as presbycusis, is the most common sensory impairment seen in the elderly. As our cochlea, the peripheral organ of hearing, ages, we tend to experience a decline in hearing and are at greater risk of cochlear sensory-neural cell degeneration and exacerbated age-related hearing impairments, e.g., gradual hearing loss, deterioration in speech comprehension (especially in noisy environments), difficulty in the localization sound sources, and ringing sensations in the ears. However, the aging process does not affect people uniformly; nor, in fact, does the aging process appear to be uniform even within an individual. Here, we outline recent research into chronological cochlear age in healthy people, and exacerbated hearing impairments during aging due to both extrinsic factors including noise and ototoxic medication, and intrinsic factors such as genetic predisposition, epigenetic factors, and aging. We review our current understanding of molecular pathways mediating ARHL and discuss recent discoveries in experimental hearing restoration and future prospects.

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“…Auditory-evoked brainstem response (ABR) thresholds were tested in accord with the methods described previously [ 15 , 16 ]. The mice at the age of the 3rd, the 4th, the 6th, and the 8th week in the control group (n=14 for all the time points) and mNGF group (n=12 for all the time points) were subjected to the measurement.…”

Section: Methodsmentioning

confidence: 99%

Hearing Improvement in A/J Mice via the Mouse Nerve Growth Factor

Gao

Xie

et al. 2017

Clin Exp Otorhinolaryngol

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Objectives To investigate the otoprotective effects of mouse nerve growth factor (mNGF) in A/J mice.Methods The mice at postnatal day 7 (P7) were randomly separated into a mNGF treated group (mNGF group) and a distilled water (for injection) treated group (control group). The mNGF dissolved in distilled water or distilled water alone was given to the mice once every other day from P7 by intramuscular injection in the hips. The otoprotective effects of mNGF in A/J mice were observed in a time course manner. The thresholds of auditory-evoked brainstem response (ABR) were tested from the age of the 3rd to the 8th week. Sections of the inner ears were stained by hematoxylin and eosin, and spiral ganglion neurons (SGNs) were observed at the age of the 3rd, the 6th,and the 8th week. Counts of whole mount outer hair cells (OHCs) in the cochleae were made at the age of 8 weeks. Expression of apoptosis related genes was determined by quantitative real-time polymerase chain reaction and Western blotting.Results ABR thresholds of the mNGF group were significantly lower than those of the control group at the age of the 6th and the 8th week. Moreover, the mNGF preserved OHC and SGN in the mouse cochleae in this period. Further experiments showed that the expression of caspase genes (including caspase-3) was inhibited in the mouse inner ears in the mNGF group.Conclusion The mNGF improves hearing in A/J mice by preserving SGN and OHC in the cochleae.

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Attenuation of hearing loss in DBA/2J mice by anti-apoptotic treatment

Cited by 17 publications

References 35 publications

Otoprotective effects of mouse nerve growth factor in DBA/2J mice with early‐onset progressive hearing loss

Otoprotective effects of mouse nerve growth factor in DBA/2J mice with early‐onset progressive hearing loss

Presbycusis: An Update on Cochlear Mechanisms and Therapies

Hearing Improvement in A/J Mice via the Mouse Nerve Growth Factor

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