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c-Myb knockdown increases the neomycin-induced damage to hair-cell-like HEI-OC1 cells in vitro.

Authors :
Yu X
Liu W
Fan Z
Qian F
Zhang D
Han Y
Xu L
Sun G
Qi J
Zhang S
Tang M
Li J
Chai R
Wang H
Source :
Scientific reports [Sci Rep] 2017 Jan 23; Vol. 7, pp. 41094. Date of Electronic Publication: 2017 Jan 23.
Publication Year :
2017

Abstract

c-Myb is a transcription factor that plays a key role in cell proliferation, differentiation, and apoptosis. It has been reported that c-Myb is expressed within the chicken otic placode, but whether c-Myb exists in the mammalian cochlea, and how it exerts its effects, has not been explored yet. Here, we investigated the expression of c-Myb in the postnatal mouse cochlea and HEI-OC1 cells and found that c-Myb was expressed in the hair cells (HCs) of mouse cochlea as well as in cultured HEI-OC1 cells. Next, we demonstrated that c-Myb expression was decreased in response to neomycin treatment in both cochlear HCs and HEI-OC1 cells, suggesting an otoprotective role for c-Myb. We then knocked down c-Myb expression with shRNA transfection in HEI-OC1 cells and found that c-Myb knockdown decreased cell viability, increased expression of pro-apoptotic factors, and enhanced cell apoptosis after neomycin insult. Mechanistic studies revealed that c-Myb knockdown increased cellular levels of reactive oxygen species and decreased Bcl-2 expression, both of which are likely to be responsible for the increased sensitivity of c-Myb knockdown cells to neomycin. This study provides evidence that c-Myb might serve as a new target for the prevention of aminoglycoside-induced HC loss.

Details

Language :
English
ISSN :
2045-2322
Volume :
7
Database :
MEDLINE
Journal :
Scientific reports
Publication Type :
Academic Journal
Accession number :
28112219
Full Text :
https://doi.org/10.1038/srep41094