Ciliated sensory hair cell formation and function require the F-BAR protein syndapin I and the WH2 domain-based actin nucleator Cobl

2013 ◽  
Vol 126 (17) ◽  
pp. 4059-4059
Author(s):  
S. Schuler ◽  
J. Hauptmann ◽  
B. Perner ◽  
M. M. Kessels ◽  
C. Englert ◽  
...  
Keyword(s):  
Hair Cell ◽  
Cell Formation ◽  
Sensory Hair ◽  
Sensory Hair Cell ◽  
Wh2 Domain ◽  
Actin Nucleator ◽  
And Function

Ciliated sensory hair cell formation and function require the F-BAR protein syndapin I and the WH2 domain-based actin nucleator Cobl

2012 ◽  
Vol 126 (1) ◽  
pp. 196-208 ◽  
Author(s):  
Susann Schüler ◽  
Judith Hauptmann ◽  
Birgit Perner ◽  
Michael M. Kessels ◽  
Christoph Englert ◽  
...  
Keyword(s):  
Hair Cell ◽  
Cell Formation ◽  
Sensory Hair ◽  
Sensory Hair Cell ◽  
Wh2 Domain ◽  
Actin Nucleator ◽  
And Function

scholarly journals MiR-210 promotes sensory hair cell formation in the organ of corti

BMC Genomics ◽  
2016 ◽  
Vol 17 (1) ◽  
Author(s):  
Sabrina Riccardi ◽  
Sebastian Bergling ◽  
Frederic Sigoillot ◽  
Martin Beibel ◽  
Annick Werner ◽  
...  
Keyword(s):  
Hair Cell ◽  
Cell Formation ◽  
Organ Of Corti ◽  
Sensory Hair ◽  
Sensory Hair Cell

scholarly journals A missense mutation in DCDC2 causes human recessive deafness DFNB66, likely by interfering with sensory hair cell and supporting cell cilia length regulation

2015 ◽  
Vol 24 (9) ◽  
pp. 2482-2491 ◽  
Author(s):  
M'hamed Grati ◽  
Imen Chakchouk ◽  
Qi Ma ◽  
Mariem Bensaid ◽  
Alexandra Desmidt ◽  
...  
Keyword(s):  
Hair Cell ◽  
Missense Mutation ◽  
Supporting Cell ◽  
Sensory Hair ◽  
Sensory Hair Cell ◽  
Length Regulation

scholarly journals Dimethyl Sulfoxide (DMSO) Exacerbates Cisplatin-induced Sensory Hair Cell Death in Zebrafish (Danio rerio)

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e55359 ◽  
Author(s):  
Phillip M. Uribe ◽  
Melissa A. Mueller ◽  
Julia S. Gleichman ◽  
Matthew D. Kramer ◽  
Qi Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Hair Cell ◽  
Dimethyl Sulfoxide ◽  
Danio Rerio ◽  
Sensory Hair ◽  
Hair Cell Death ◽  
Sensory Hair Cell

scholarly journals Oral Antioxidant Vitamins and Magnesium Limit Noise-Induced Hearing Loss by Promoting Sensory Hair Cell Survival: Role of Antioxidant Enzymes and Apoptosis Genes

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1177
Author(s):  
Juan C. Alvarado ◽  
Verónica Fuentes-Santamaría ◽  
Pedro Melgar-Rojas ◽  
María C. Gabaldón-Ull ◽  
José J. Cabanes-Sanchis ◽  
...  
Keyword(s):  
Cell Death ◽  
Hearing Loss ◽  
Antioxidant Enzymes ◽  
Oral Administration ◽  
Hair Cell ◽  
Cell Survival ◽  
Sensory Cell ◽  
Auditory Function ◽  
Sensory Hair ◽  
Sensory Hair Cell

Noise induces oxidative stress in the cochlea followed by sensory cell death and hearing loss. The proof of principle that injections of antioxidant vitamins and Mg2+ prevent noise-induced hearing loss (NIHL) has been established. However, effectiveness of oral administration remains controversial and otoprotection mechanisms are unclear. Using auditory evoked potentials, quantitative PCR, and immunocytochemistry, we explored effects of oral administration of vitamins A, C, E, and Mg2+ (ACEMg) on auditory function and sensory cell survival following NIHL in rats. Oral ACEMg reduced auditory thresholds shifts after NIHL. Improved auditory function correlated with increased survival of sensory outer hair cells. In parallel, oral ACEMg modulated the expression timeline of antioxidant enzymes in the cochlea after NIHL. There was increased expression of glutathione peroxidase-1 and catalase at 1 and 10 days, respectively. Also, pro-apoptotic caspase-3 and Bax levels were diminished in ACEMg-treated rats, at 10 and 30 days, respectively, following noise overstimulation, whereas, at day 10 after noise exposure, the levels of anti-apoptotic Bcl-2, were significantly increased. Therefore, oral ACEMg improves auditory function by limiting sensory hair cell death in the auditory receptor following NIHL. Regulation of the expression of antioxidant enzymes and apoptosis-related proteins in cochlear structures is involved in such an otoprotective mechanism.

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