Anttonen, Tommi Miikael

[["dc.bibliographiccitation.artnumber","ENEURO.0047"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","eNeuro"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Anttonen, Tommi"],["dc.contributor.author","Herranen, Anni"],["dc.contributor.author","Virkkala, Jussi"],["dc.contributor.author","Kirjavainen, Anna"],["dc.contributor.author","Elomaa, Pinja"],["dc.contributor.author","Laos, Maarja"],["dc.contributor.author","Liang, Xingqun"],["dc.contributor.author","Ylikoski, Jukka"],["dc.contributor.author","Behrens, Axel"],["dc.contributor.author","Pirvola, Ulla"],["dc.date.accessioned","2019-01-24T11:54:14Z"],["dc.date.available","2019-01-24T11:54:14Z"],["dc.date.issued","2016"],["dc.description.abstract","Prevention of auditory hair cell death offers therapeutic potential to rescue hearing. Pharmacological blockade of JNK/c-Jun signaling attenuates injury-induced hair cell loss, but with unsolved mechanisms. We have characterized the c-Jun stress response in the mouse cochlea challenged with acoustic overstimulation and ototoxins, by studying the dynamics of c-Jun N-terminal phosphorylation. It occurred acutely in glial-like supporting cells, inner hair cells, and the cells of the cochlear ion trafficking route, and was rapidly downregulated after exposures. Notably, death-prone outer hair cells lacked c-Jun phosphorylation. As phosphorylation was triggered also by nontraumatic noise levels and none of the cells showing this activation were lost, c-Jun phosphorylation is a biomarker for cochlear stress rather than an indicator of a death-prone fate of hair cells. Preconditioning with a mild noise exposure before a stronger traumatizing noise exposure attenuated the cochlear c-Jun stress response, suggesting that the known protective effect of sound preconditioning on hearing is linked to suppression of c-Jun activation. Finally, mice with mutations in the c-Jun N-terminal phosphoacceptor sites showed partial, but significant, hair cell protection. These data identify the c-Jun stress response as a paracrine mechanism that mediates outer hair cell death."],["dc.identifier.doi","10.1523/ENEURO.0047-16.2016"],["dc.identifier.pmid","27257624"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57359"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","2373-2822"],["dc.title","c-Jun N-Terminal Phosphorylation: Biomarker for Cellular Stress Rather than Cell Death in the Injured Cochlea"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]