Steroidogenic Enzyme Expression in the Rat Cochlea

Abstract

Objective—Steroid hormones, and particularly mineralocorticoids, are candidates for controlling the homeostasis of endolymph as steroid receptors are widely expressed in the cochlea. In contrast, experiments on adrenalectomized animals have shown that an absence of steroids had little effect on the ionic composition of endolymph and hearing ability. We thus hypothesized that local production of steroids in the inner ear may regulate cochlear fluid exchanges.Results—Using reverse transcription-polymerase chain reaction techniques, we showed that transcripts encoding the P450 side-chain cleavage, the 3β hydroxysteroid dehydrogenase (3β HSD) and the 17α hydroxylase (P450 C17) were expressed in the lateral wall, organ of Corti and modiolus. The mRNA encoding aldosterone synthase was expressed in the modiolus and lateral wall while the P450 11β1 hydroxylase was not detected at all in any of these tissues. In situ hybridization experiments on cochlear sections confirmed that the 3β HSD transcripts were expressed in the spiral ligament and modiolus and possibly in the hair cells of the organ of Corti. However, it was not possible to detect P450 C17 transcripts. Immunohistochemistry performed with an antibody raised against the various 3β HSD isoforms confirmed the localization found using in situ hybridization.Conclusions—These results suggest that enzymes of the steroid pathway leading to mineralocorticoids and sex steroid hormones, but not glucocorticoids, may be expressed in the rat cochlea. This work is in line with the recent description of local production of steroid hormones in the brain (neurosteroids), heart and skin. In the cochlea, the local production of mineralo and sex steroids could account for a paracrine role and could induce specific gene expression through steroid receptors or act via a non-genomic mechanism on membrane receptors or ionic exchangers. Experiments aimed at demonstrating enzymatic activities within cochlea tissues are in progress.