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ABSTRACT: Introduction
Cochlear injury activates the resident macrophages (RM) and recruits the blood-circulating monocytes and monocyte-derived macrophages (Mo/Mo-M), but their specific functions in the injured cochlea are unknown. It is well-established that the chemokine fractalkine receptor (CX3CR1), expressed by cochlear macrophages, influences the density of those macrophages and promotes synaptic repair and spiral ganglion neuron (SGN) survival in the injured cochlea. As CX3CR1 is expressed on both RM and Mo/Mo-M, it remains unclear if CX3CR1- expressing RM and Mo/Mo-M are distinct and differentially promote SGN survival after cochlear injury.Methods
We used a fate mapping tamoxifen-inducible CX3CR1 mouse model (CX3CR1
SUBMITTER: Murali SV
PROVIDER: S-EPMC12492497 | biostudies-literature | 2025
REPOSITORIES: biostudies-literature