Metabolic reprogramming of inner ear cell line HEI-OC1 after dexamethasone application

Introduction One approach to dampen the inflammatory reactions resulting from implantation surgery of cochlear implant hearing aids is to embed dexamethasone into the matrix of the electrode carrier. Possible side effects for sensory cells in the inner ear on the metabolomics have not yet been evaluated. Objective We examined changes in the metabolome of the HEI-OC1 cell line after dexamethasone incubation as a cell model of sensory cells of the inner ear. Results and Conclusion Untargeted GC-MS-profiling of metabolic alterations after dexamethasone treatment showed that dexamethasone had antithetical effects on the metabolic signature of the cells depending on growth conditions. The differentiated state of HEI-OC1 cells is better suited for elucidating metabolic changes induced by external factors. Dexamethasone treatment of differentiated cells led to an increase in intracellular amino acids and enhanced glucose uptake and beta-oxidation in the cells. Increased availability of precursors for glycolysis and ATP production by beta-oxidation stabilizes the energy supply in the cells, which could be assumed to be beneficial in coping with cellular stress. We found no negative effects of dexamethasone on the metabolic level, and changes may even prepare sensory cells to better overcome cellular stress following implantation surgery.

Automated summary

Embedding dexamethasone into the matrix of the electrode carrier can help reduce inflammatory reactions in sensory cells following cochlear implantation surgery. Research on changes in the metabolome of HEI-OC1 cells after dexamethasone incubation showed that dexamethasone treatment can increase intracellular amino acids, enhance glucose uptake, and beta-oxidation to stabilize energy supply in cells. This preparation may benefit sensory cells in coping with cellular stress post-implantation surgery.