Vibration induced hearing loss in guinea pig cochlea: expression of TNF-α and VEGF

Zou, Jing; Pyykkö, Ilmari; Sutinen, Päivi; Toppila, Esko

doi:10.1016/j.heares.2004.10.008

Cited by 69 publications

(66 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Its function in neuroprotection and plasticity may be mediated by tumor necrosis factor receptor-2 (TNFR2) and the activation of downstream pathways involving NF-κB (Dolga et al 2008;Pradillo et al 2009). TNFR2 is widely induced in structures of the mature cochlea after noxious stimuli (Zou et al 2005) and the NF-κB pathway is protective against ototoxic insults to the cochlea (Jiang et al 2005). In the absence of overt stress, however, the TNF-α knock-out mice in this study showed normal synapses and neurons.…”

Section: Discussionmentioning

confidence: 55%

“…Specifically, TNF-α is produced by spiral ligament fibrocytes, outer hair cells, and supporting cells within the organ of Corti following noise exposure, excessive vibration, or treatment with cisplatin (Zou et al 2005, Fujioka et al 2006, Moon et al 2006, So et al 2007, Park et al 2009). Further supporting a pro-inflammatory role for TNF-α in cochlear injury and repair is the fact that the infusion of TNF-α into the guinea pig cochlea leads to the infiltration of inflammatory cells, such as leukocytes, and that the number of cochlear macrophages increases following acoustic trauma (Hirose et al 2005, Keithley et al 2008.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Tumor Necrosis Factor-alpha-mutant Mice Exhibit High Frequency Hearing Loss

Oishi

Zheng

Hill

et al. 2013

JARO

View full text Add to dashboard Cite

Exogenous tumor necrosis factor-alpha (TNF-α) plays a role in auditory hair cell death by altering the expression of apoptosis-related genes in response to noxious stimuli. Little is known, however, about the function of TNF-α in normal hair cell physiology. We, therefore, investigated the cochlear morphology and auditory function of TNF-α-deficient mice. Auditory evoked brainstem response showed significantly higher thresholds, especially at higher frequencies, in 1-month-old TNF-α −/− mice as compared to TNF-α +/− and wild type (WT); hearing loss did not progress further from 1 to 4 months of age. There was no difference in the gross morphology of the organ of Corti, lateral wall, and spiral ganglion cells in TNF-α −/− mice compared to WT mice at 4 months of age, nor were there differences in the anatomy of the auditory ossicles. Outer hair cells were completely intact in surface preparations of the organ of Corti of TNF-α −/− mice, and synaptic ribbon counts of TNF-α −/− and WT mice at 4 months of age were similar. Reduced amplitudes of distortion product otoacoustic emissions, however, indicated dysfunction of outer hair cells in TNF-α −/− mice. Scanning electron microscopy revealed that stereocilia were sporadically absent in the basal turn and distorted in the middle turn. In summary, our results demonstrate that TNF-α-mutant mice exhibit early hearing loss, especially at higher frequencies, and that loss or malformation of the stereocilia of outer hair cells appears to be a contributing factor.

show abstract

Section: Discussionmentioning

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Tumor Necrosis Factor-alpha-mutant Mice Exhibit High Frequency Hearing Loss

Oishi

Zheng

Hill

et al. 2013

JARO

View full text Add to dashboard Cite

show abstract

“…For example, RANTES/CCL1 (Bolin et al, 1998) and tumor necrosis factor (TNF) (Bianchi et al, 2005), as well as the receptors CCR1 (for RANTES) and CXCR4/2 (for MIF) (Bernhagen et al, 2007) and TNFR1/2 (also known as TNFRSF1A/B) (Zou et al, 2005), are found in the inner ear. Another MIF receptor, CD44, is expressed in pillar cells (Hertzano et al, 2010) in developing and adult inner ear tissues.…”

Section: Research Article Development 139 (24)mentioning

confidence: 99%

Macrophage migration inhibitory factor acts as a neurotrophin in the developing inner ear

et al. 2012

View full text Add to dashboard Cite

This study is the first to demonstrate that macrophage migration inhibitory factor (MIF), an immune system ‘inflammatory’ cytokine that is released by the developing otocyst, plays a role in regulating early innervation of the mouse and chick inner ear. We demonstrate that MIF is a major bioactive component of the previously uncharacterized otocyst-derived factor, which directs initial neurite outgrowth from the statoacoustic ganglion (SAG) to the developing inner ear. Recombinant MIF acts as a neurotrophin in promoting both SAG directional neurite outgrowth and neuronal survival and is expressed in both the developing and mature inner ear of chick and mouse. A MIF receptor, CD74, is found on both embryonic SAG neurons and adult mouse spiral ganglion neurons. Mif knockout mice are hearing impaired and demonstrate altered innervation to the organ of Corti, as well as fewer sensory hair cells. Furthermore, mouse embryonic stem cells become neuron-like when exposed to picomolar levels of MIF, suggesting the general importance of this cytokine in neural development.

show abstract

“…As described above, steroids also regulate interactions with the transcription factors TNFα and AP-1, and inhibit NOS. TNFα (Satoh et al, 2002;Aminpour et al, 2005;Zou et al, 2005), AP-1 (Ogita et al, 2000;Shizuki et al, 2002;Matsunobu et al, 2004;Nagashima et al, 2005), and NOS (Hess et al, 1999;Ohinata et al, 2003;Yamane et al, 2004;Chen et al, 2005) have all been implicated in the cochlear response to stress. Thus, the specific mechanism(s) of action of dexamethasone in prevention of NIHL remain to be precisely identified.…”

Section: Growth Factorsmentioning

confidence: 99%

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

et al. 2007

View full text Add to dashboard Cite

Recent research has shown the essential role of reduced blood flow and free radical formation in the cochlea in noise-induced hearing loss (NIHL). The amount, distribution, and time course of free radical formation have been defined, including a clinically significant late formation 7-10 days following noise exposure, and one mechanism underlying noise-induced reduction in cochlear blood flow has finally been identified. These new insights have led to the formulation of new hypotheses regarding the molecular mechanisms of NIHL; and, from these, we have identified interventions that prevent NIHL, even with treatment onset delayed up to 3 days post-noise. It is essential to now assess the additive effects of agents intervening at different points in the cell death pathway to optimize treatment efficacy. Finding safe and effective interventions that attenuate NIHL will provide a compelling scientific rationale to justify human trials to eliminate this single major cause of acquired hearing loss.

show abstract

Vibration induced hearing loss in guinea pig cochlea: expression of TNF-α and VEGF

Cited by 69 publications

References 27 publications

Tumor Necrosis Factor-alpha-mutant Mice Exhibit High Frequency Hearing Loss

Tumor Necrosis Factor-alpha-mutant Mice Exhibit High Frequency Hearing Loss

Macrophage migration inhibitory factor acts as a neurotrophin in the developing inner ear

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

Contact Info

Product

Resources

About