The redox protein p66shc mediates cochlear vascular dysfunction and transient noise-induced hearing loss

• DOI: 10.1038/srep25450
• Publication Date: 2016-05-09T09:10:13Z
• Authors: A. R. Fetoni; S. L. M. Eramo; F. Paciello; R. Rolesi; D. Samengo; G. Paludetti; D. Troiani; G. Pani
• Keywords: Spiral ganglion; Endothelial Dysfunction; Noise-induced hearing loss

Abstract p66 shc , a member of the ShcA protein family, is essential for cellular response to oxidative stress, and elicits formation mitochondrial Reactive Oxygen Species (ROS), thus promoting vasomotor dysfunction inflammation. Accordingly, mice lacking isoform display increased resistance tissue damage cardiovascular disorders. Oxidative stress also contributes noise-induced hearing loss (NIHL); we found that expression serine phosphorylation were induced following noise exposure in rat cochlea, together with markers inflammation ischemia as indicated by levels hypoxic inducible factor (HIF) vascular endothelial growth (VEGF) highly vascularised cochlear lateral region spiral ganglion. Importantly, knock-out (p66 KO) 126 SvEv adult less vulnerable acoustic trauma respect wild type controls, shown preserved auditory function remarkably lower markers. Of note, decline observed 12 month old WT controls was markedly attenuated p66KO consistent delayed inner ear senescence. Collectively, have identified pivotal role -induced common pathogenic cascade shared age-related loss.