title: Immune defense is the primary function associated with the differentially expressed genes in the cochlea following acoustic trauma.
abstract: Our previous RNA-sequencing analysis of the rat cochlear genes identified multiple biological processes and molecular pathways in the cochlear response to acoustic overstimulation. However, the biological processes and molecular pathways that are common to other species have not been documented. The identification of these common stress processes is pivotal for a better understanding of the essential response of the cochlea to acoustic injury. Here, we compared the RNA-sequencing data collected from mice and rats that sustained a similar, but not identical, acoustic injury. The transcriptome analysis of cochlear genes identified the differentially expressed genes in the mouse and rat samples. Bioinformatics analysis revealed a marked similarity in the changes in the biological processes between the two species, although the differentially expressed genes did not overlap well. The common processes associated with the differentially expressed genes are primarily associated with immunity and inflammation, which include the immune response, response to wounding, the defense response, chemotaxis and inflammatory responses. Moreover, analysis of the molecular pathways showed considerable overlap between the two species. The common pathways include cytokine-cytokine receptor interactions, the chemokine signaling pathway, the Toll-like receptor signaling pathway, and the NOD-like receptor signaling pathway. Further analysis of the transcriptional regulators revealed common upstream regulators of the differentially expressed genes, and these upstream regulators are also functionally related to the immune and inflammatory responses. These results suggest that the immune and inflammatory responses are the essential responses to acoustic overstimulation in the cochlea.
authors.affiliation: Center for Hearing and Deafness, University at Buffalo, NY 14214, USA. Electronic address: qits-002@163.com.
authors.forename: Shuzhi
authors.initials: S
authors.lastname: Yang
authors.affiliation: Center for Hearing and Deafness, University at Buffalo, NY 14214, USA. Electronic address: qunfengcai@gmail.com.
authors.forename: Qunfeng
authors.initials: Q
authors.lastname: Cai
authors.affiliation: Center for Hearing and Deafness, University at Buffalo, NY 14214, USA. Electronic address: rvr@buffalo.edu.
authors.forename: R Robert
authors.initials: RR
authors.lastname: Vethanayagam
authors.affiliation: Department of Biostatistics and Bioinformatics, Roswell Park Cancer Institute, Elm & Carlton Streets, Buffalo, NY 14263, USA. Electronic address: Jianmin.Wang@RoswellPark.org.
authors.forename: Jianmin
authors.initials: J
authors.lastname: Wang
authors.affiliation: Center for Hearing and Deafness, University at Buffalo, NY 14214, USA. Electronic address: yangwp301@126.com.
authors.forename: Weiping
authors.initials: W
authors.lastname: Yang
authors.affiliation: Center for Hearing and Deafness, University at Buffalo, NY 14214, USA. Electronic address: bhu@buffalo.edu.
authors.forename: Bo Hua
authors.initials: BH
authors.lastname: Hu
mesh_terms: D000818:Animals; D003051:Cochlea / Q000276:immunology* / Q000503:physiopathology; D019295:Computational Biology; D030541:Databases, Genetic; D004195:Disease Models, Animal; D005260:Female; D020869:Gene Expression Profiling / Q000379:methods; D005786:Gene Expression Regulation; D006317:Hearing Loss, Noise-Induced / Q000235:genetics* / Q000276:immunology* / Q000503:physiopathology; D008297:Male; D008808:Mice, Inbred CBA; D009622:Noise / Q000009:adverse effects*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D017423:Sequence Analysis, RNA; D059467:Transcriptome
chemical_list: D012333:RNA, Messenger
keywords: Inner ear; Noise; RNA-sequencing; Transcriptome