Journal
SCIENTIFIC REPORTS
Volume 7, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep41094
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Funding
- National 973 Basic Research Program of China [2014CB541703, 2015CB965000]
- National Natural Science Foundation of China [81570918, 81200744, 81622013, 81470692, 81500790, 81570921, 31500852, 31501194]
- Shandong Provincial Natural Science Foundation, China [ZR2014HQ076]
- Key Project of Shandong Provincial Programs for Research and Development [2015GSF118153]
- Natural Science Foundation of Jiangsu Province [BK20150022, BK20140620, BK20150598]
- Yingdong Huo education foundation
- Fundamental Research Funds for the Central Universities [2242014R30022, 021414380037]
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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.
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