The influence of loud sound stress on expression of osmotic stress protein 94 in the murine inner ear.

Osmotic stress protein 94 (OSP94), a member of the heat shock protein 110/SSE subfamily, is expressed in certain organs such as the kidney, testis, and brain where it can act as a molecular chaperon. In general, its alteration in expression is in response to hyper-ionic and osmotic stress as well as heat shock stress. Since many cells in the inner ear are involved in active ion transportation and are constantly exposed to two ionic different environments, we hypothesize that OSP94 may be expressed in the inner ear and its expression may be influenced by loud sound stress (LSS). With immunohistochemistry combined with confocal microscopy, immunoblotting, and reverse transcription polymerase chain reaction techniques, we found that OSP94 was widely expressed in various cells in the murine cochlea including the stria vascularis, the organ of Corti, the interdental cells, spiral ganglion cells, the spiral ligament, and Reissner's membrane. Under the unstressed condition, the transcription and protein level of OSP94 expression in the inner ear was quantitatively similar to that of the kidney. Furthermore, its expression in the inner ear by LSS from broadband noise at 117 dB/SPL was upregulated, but remained unchanged in the kidney. In particular, the upregulation of OSP94 in the cochlear lateral wall tissue was slowly elicited in a LSS time-dependent manner compared with the response of two other HSPs; HSP25 and HSP70 are considered to play a cytoprotective role under stressful conditions. Our results show that OSP94 is expressed in the inner ear and indicate this may be necessary for cells in a special ionic and osmotic environment such as endo-perilymphatic ion compartments. The organ-specific upregulation of OSP94 by acoustic overstimulation reveals that OSP94 in the murine inner ear is potentially important for cellular functional adaptation to LSS.