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Investigation of Notch Signaling during Spontaneous Regeneration of Cochlear Hair Cells

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Technical Report,15 Sep 2015,14 Sep 2016

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Southern Illinois University School of Medicine Springfield United States

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Hearing loss and tinnitus commonly occur after exposure to intense or prolonged levels of loud noise which are inherent to military settings. These noise exposures damage and kill sensory hair cells HCs found in the cochlea of the inner ear, resulting in permanent hearing loss and tinnitus. Regeneration of auditory HCs and recovery of hearing function naturally occurs in non-mammalian vertebrates. In contrast, auditory HCs are not replaced after damage in humans and other mature mammals. However, we have recently discovered that the neonatal mouse cochlea is capable of spontaneous HC regeneration. Understanding the molecular mechanism that allows spontaneous HC regeneration to occur in neonatal mice is the first step to stimulating successful HC regeneration in adults and translating these findings to humans who suffer from hearing loss. Our central hypothesis is that following HC damage in the neonatal mouse cochlea, Notch-mediated lateral inhibition is removed which causes a decrease in Notch signaling in supporting cells, allowing them to change cell fate and become HCs. We are also investigating the relationship between individual Notch ligands and target genes in the undamaged, neonatal cochlea to understand which ones control supporting cell to HC conversion. Data collected from year 1 of this award shows changes in Notch signaling following HC damage in the neonatal mouse cochlea using different techniques. Interestingly we observed loss of Notch signaling in three supporting cell subtypes pillar cells, Deiters cells and Hensen cells, but not in other subtypes. We also present preliminary data on the effect of deleting the Notch ligand Jagged1 from supporting cells in the neonatal, undamaged cochlea.

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  • Medicine and Medical Research

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