Upregulation of HSP60 expression in the postnatal rat cochlea and rats with drug-induced hearing loss

Abstract

Heat shock protein 60 (HSP60) is a highly conserved chaperone molecule that plays important roles in mediating some physiological and pathological functions. However, researchers have not yet determined whether HSP60 is expressed in the mammalian cochlea. This study constitutes the first investigation of the expression of HSP60 in the postnatal rat cochlea. We also examined the expression of HSP60 in rats with drug-induced hearing loss. Auditory thresholds were assessed by monitoring the auditory brainstem response (ABR) prior to and after drug injection. Expression levels of the HSP60 gene (Hsp60) and HSP60 protein in the rat cochlea were detected by quantitative real-time polymerase chain reaction and Western blotting, respectively. The distribution of HSP60 in the rat cochlea was further examined by immunofluorescence staining. We have demonstrated that HSP60 was expressed in the postnatal rat cochlea in an age-dependent and cell-specific manner. In addition, after drug exposure, the average hearing threshold of rats in the experimental group was significantly higher than that in the control group, with increased HSP60 expression level in response to kanamycin and furosemide treatments. HSP60 expression was observed in the supporting cells (SCs) within the organ of Corti in both the uninjured and the injured cochlea, but it was undetectable in the mechanosensory hair cells (HCs) and spiral ganglion neurons. Therefore, our research suggests that HSP60 may play an important role in auditory function.