Examining the Relationship between Alpha-Parvalbumin and Oncomodulin: A Pilot Study on the Calcium-Binding Proteins of the Inner Ear
The regulation of calcium (Ca2+) is essential to the proper function of outer hair cells (OHCs) in the mammalian cochlea. Trauma and aging are known to disrupt Ca2+ signaling as well as cause the malfunction of OHCs. Therefore, Ca2+ signaling may be strongly linked to the viability of OHCs. In both mice and humans two calcium-binding proteins are highly expressed during development of hearing and during aging: oncomodulin (OCM) and alpha-parvalbumin (aPV). These mobile Ca2+ buffers are EF-hand binding proteins, consisting of helix-loop-helix domains. Despite their similar structure and function, we hypothesize that in the absence of OCM, aPV plays little or no role in OHC function. To test this hypothesis, we performed distortion product otoacoustic emissions (DPOAE) assays on mice with a single knockout (SKO) of OCM as well as on mice with a double knockout (DKO) of both OCM and aPV. Results from this pilot study suggest that there is no significant difference in age-related hearing loss between the SKO and DKO mouse phenotypes. However, increased aPV expression in response to a lack of OCM remains to be investigated.