Heat-stress Actuated Protective Mechanism of the Inner Ear against Noise-induced Hearing Loss

Noise-induced hearing loss (NIHL) is irreversible damage to the ear caused by traumatic noise exposure. This is mainly due to mechanical damage to outer hair cells (OHCs), a type of sensory cell in the inner ear. Recently, prior conditioning with sublethal stressors has been reported to protect the inner ear from acoustic injury, realizing less hearing loss. To explore the stress-actuated protective mechanism of the inner ear against NIHL, the mechanical properties and the amount of filamentous actin (F-actin) of mouse OHCs were investigated before and after conditioning with heat stress. In addition, expression of heat shock protein 27 (HSP27) in the cochlea, which affects the formation of F-actin, was investigated. Heat stress caused an increase in Young’s modulus of OHCs at 3–6 h after its application along with an increase in their amount of F-actin. This time course is similar to that found in a previous study in which heat stress was shown to suppress permanent threshold shift. Heat stress was also found to increase HSP27 in the cochlea. These results suggest that heat stress induces HSP27 expression and thus increases F-actin in OHCs, increasing their stiffness, resulting in protection of the ear against NIHL. INTRODUCTION Outer hair cells (OHCs) of the mammalian cochlea are capable of altering their cell length in response to changes in membrane potential, termed electromotility [1]. Due to this electromotility, OHCs can exert force on the basilar membrane, which results in cochlear amplification (Fig. 1). As a result, hearing in mammals is characterized by high sensitivity, wide dynamic range and sharp frequency selectivity. Unfortunately, however, they are susceptible to external stimuli. Hence, if the ear is overexposed to sufficiently intense and/or prolonged sound, Figure 1.Human auditory system. OHCs are located on the basilar membrane in the cochlea and subject the membrane to force, leading to cochlear amplification. The cytoskeleton of the OHC consists of parallelly arranged F-actin and spectrin which cross-links the adjacent actin filaments.