Ca2+ Dysregulation Affects Mitochondrial Morphology in Outer Hair Cells




Basoor, Sinchana

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The normal function of outer hair cells (OHCs) of the cochlea requires a delicate regulation of calcium (Ca2+). Prolonged excessive noise and aging can disrupt this regulation and result in oxidative stress. Oncomodulin (OCM) is the prevalent calcium-binding protein in mammalian cochleae and its presence may moderate the damage caused by injurious stimuli, such as noise. Mitochondria play a central role in oxidative stress and can show signs of stress through changes in their dynamic morphology (size and shape). We hypothesize that a lack of OCM or noise exposure results in distinct changes to the mitochondrial networks of OHCs which may contribute to their dysfunction prior to cell death. To test this, distortion product otoacoustic emissions (DPOAE) assays on wildtype mice and mice lacking OCM were performed to assess hearing ability. Immunofluorescence was performed on cochlear sections to label mitochondria and OHCs for morphology analysis using the Imaris program. Results from these preliminary experiments show that OHCs from mice exposed to noise or lacking OCM exhibit increased hearing thresholds and distinct changes in the mitochondrial morphology of their outer hair cells.



Biology, Hearing Loss, Mitochondria, Calcium, Oncomodulin