2017 Volume 68 Pages 1-7
The most common reason for sensorineural hearing loss is death of hair cells (HC) from diverse stressors. When HC degenerate they are not replaced, and therefore hearing loss is permanent. Heat shock proteins (HSPs) are molecular chaperones, participating in folding, targeting and degrading proteins in all cells. In addition, HSP expression is increased in response to various environmental stresses to protect cells from damage. One common HSP, HSP70, inhibits apoptosis caused by heat shock and other stresses. Here we test whether Adenovirus with HSP
70 (Ad.HSP70) gene transfer protects against a systemic ototoxic insult (kanamycin and furosemide combination) in the guinea pig cochlea, in vivo. In addition, we invested where HSP70 expresses in cochlea by HSP70 staining. Ad.HSP70-mCherry was injected to experimental animals and Ad.mCherry to controls, 4 days prior to the ototoxic insult. Hearing thresholds were measured by ABR before the insult and again prior to sacrificing the animals, 14 days after the insult. Epi-fluorescence immunocytochemistry showed that injection of Ad.HSP70-mCherry resulted in mCherry fluorescence in non-sensory cells of the organ of Corti. The ototoxic insult eliminated both outer HCs (OHCs) and inner HCs (IHCs) throughout most of the cochlea of control (Ad.mCherry-injected) ears and contralateral (un-injected) ears. Ad.HSP70-mCherry-injected ears exhibited a significant preservation of IHCs compared to control and contralateral ears. ABR thresholds were significantly better in Ad.HSP70-mCherry-injected ears than in control and contralateral ears. Our data showed that HSP70 expression was found to be in harmony with mCherry expression in non-sensory cells of cochlea.