PGC-1α affects cochlear pericytes migration in noise-exposed mice

Objective: The study aimed to observe the effects of noise exposure on the pericytes of the cochlear stria vascularis (SV) in mice and to investigate its molecular mechanism.Method: Male C57BL/6J mice aged 6-8 weeks were used as the subjects. Auditory Brainstem Response (ABR) was used to assess hearing loss. Hematoxylin and Eosin (HE) staining was conducted to observe morphological alterations in the SV. Immunofluorescence combined with transmission electron microscopy (TEM) was used to scrutinize changes in pericytes following acoustic injury. Western blotting (WB) was used to assess the expression variations of the migration-related protein Osteopontin (OPN). Evans Blue assay was performed to evaluate the permeability of the blood labyrinth barrier (BLB). 4-Hydroxynonenal (4-HNE) staining, in conjunction with measurements of Superoxide Dismutase (SOD), Malondialdehyde (MDA), and Catalase (CAT) content, was used to ascertain whether oxidative stress injury occurred in the SV. WB, combined with immunofluorescence, was used to examine alterations in the expression of proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1 alpha) in the SV and pericytes.Results: Noise exposure resulted in permanent hearing loss in C57BL/6J mice, accompanied by SV swelling, migration of pericytes from their vascular attachments, BLB leakage, elevated oxidative stress levels in the SV, and reduced expression of PGC-1 alpha on both the SV and migrating pericytes.Conclusion: Noise exposure may potentially increase oxidative stress levels in the SV, downregulate the expression levels of PGC-1 alpha, promote pericytes migration, and subsequently lead to an elevation in BLB permeability.

Automated summary

Noise exposure leads to hearing loss in mice, accompanied by swelling of the cochlear stria vascularis, migration of pericytes, leakage of the blood labyrinth barrier, increased oxidative stress levels in the stria vascularis, and reduced expression of PGC-1 alpha.