| ARTICLE |
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| Year : 2014 | Volume
: 16
| Issue : 73 | Page : 400--409 |
Noise exposure immediately activates cochlear mitogen-activated protein kinase signaling
Kumar N Alagramam1, Ruben Stepanyan1, Samson Jamesdaniel2, Daniel H.-C. Chen1, Rickie R Davis3
1 Department of Otolaryngology, University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, OH 44106, USA
2 Institute of Environmental Health Sciences, Wayne State University, Detroit, MI 4820, USA
3 Department of Biological Sciences, University of Cincinnati, Cincinnati, OH 45221; Division of Applied Research and Technology, National Institute for Occupational Safety and Health, Department of Health and Human Services, Cincinnati, OH 45226, USA
Correspondence Address:
Dr. Kumar N Alagramam
Department of Otolaryngology, University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, OH 44106
USA
 Source of Support: This work was supported by a grant (R21-DC07866) from the NIH to K.N.A., Conflict of Interest: None  | Check |
DOI: 10.4103/1463-1741.144418
Noise-induced hearing loss (NIHL) is a major public health issue worldwide. Uncovering the early molecular events associated with NIHL would reveal mechanisms leading to the hearing loss. Our aim is to investigate the immediate molecular responses after different levels of noise exposure and identify the common and distinct pathways that mediate NIHL. Previous work showed mice exposed to 116 decibels sound pressure level (dB SPL) broadband noise for 1 h had greater threshold shifts than the mice exposed to 110 dB SPL broadband noise, hence we used these two noise levels in this study. Groups of 4-8-week-old CBA/CaJ mice were exposed to no noise (control) or to broadband noise for 1 h, followed by transcriptome analysis of total cochlear RNA isolated immediately after noise exposure. Previously identified and novel genes were found in all data sets. Following exposure to noise at 116 dB SPL, the earliest responses included up-regulation of 243 genes and down-regulation of 61 genes, while a similar exposure at 110 dB SPL up-regulated 155 genes and down-regulated 221 genes. Bioinformatics analysis indicated that mitogen-activated protein kinase (MAPK) signaling was the major pathway in both levels of noise exposure. Nevertheless, both qualitative and quantitative differences were noticed in some MAPK signaling genes, after exposure to different noise levels. Cacna1b , Cacna1g , and Pla2g6 , related to calcium signaling were down-regulated after 110 dB SPL exposure, while the fold increase in the expression of Fos was relatively lower than what was observed after 116 dB SPL exposure. These subtle variations provide insight on the factors that may contribute to the differences in NIHL despite the activation of a common pathway.
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