Oncomodulin Alters the Ca2+-Regulating Network in Cochlear Outer Hair Cells

Abstract

The study of hair cells (HCs) located in the cochlea of the inner ear is beginning to unveil the mysteries of hearing loss. HCs transform sound waves into electrical signals that are sent to the brain for interpretation and are essential for hearing. In previous work, analysis of the expression of cytosolic calcium (Ca2+)-binding proteins (CaBPs) in HCs has illuminated potential mechanisms for the development, maintenance, and deterioration of hearing. In mice where a particular CaBP, Oncomodulin (OCM), was genetically engineered to be missing, hearing loss was accelerated. In fact, 4 months after birth, they were essentially deaf. Thus, OCM is a CaBP of interest because it is directly involved in the maintenance of hearing. To determine how OCM maintains hearing, this thesis project examined the impact that OCM had on Ca2+ regulator proteins within the outer hair cell (OHC). Data was collected using reverse transcription quantitative polymerase chain reaction (RT-qPCR) for quantitative analysis and immunohistochemistry for qualitative analysis. In OHCs, the engineered absence of OCM altered the expression of 3 purinergic receptors, 2 voltage-gated Ca2+ channels, an intracellular Ca2+ buffer, and an ATP-driven Ca2+ exporter, which suggests that OCM modulates the OHC Ca2+-regulating network in order to establish intracellular Ca2+ balance.