Rab3A attenuated H₂O₂-induced mitochondrial dysfunction and damage in HEI-OC1 cells by stabilizing ITGA3 expression.

Abstract

According to reports, Rab3A plays a kay role in various diseases. The regulatory role of Rab3A in hair cell damage and age-related hearing loss has not been explored. HEI-OC-1 cells were treated with hydrogen peroxide (H₂O₂) to construct a damage model. The cell viability and apoptosis were detected by CCK-8 assay and flow cytometry. Immunofluorescence and flow cytometry were used to measure mitochondrial membrane potential. The contents of oxidative stress-related indicators and mitochondrial function-related indicators were detected by kits. Dual luciferase assay was used to determine the regulatory relationship between Rab3A and ITGA3. The results showed that H₂O₂ treatment reduced the level of Rab3A in HEI-OC-1 cells in a time-dependent manner. Rab3A increased the cell viability of H₂O₂-induced inner ear cells and inhibited cell apoptosis. Additionally, Rab3A inhibited H₂O₂-induced oxidative stress and alleviated mitochondrial dysfunction in HEI-OC-1 cells. Rab3A also directly targeted and positively regulated ITGA3 expression. Further studies found that silencing of ITGA3 reversed the inhibitory effects of Rab3A on inner ear cell damage and mitochondrial dysfunction. In conclusion, Rab3A regulates H₂O₂-induced inner ear hair cell damage and mitochondrial dysfunction by stabilizing the expression of ITGA3.