CD93 and GAIP-interacting protein, C termius (GIPC) have been shown to interactively alter phagocytic processes of immune cells. CD93 and GIPC expression and localization during central nervous system inflammation have not yet been reported. In this study, we established a rat model of brain inflammation by lipopolysaccharide injection to the lateral ventricle. In the brain of rats with inflammation, western blots showed increased CD93 expression that decreased over time. GIPC expression was unaltered. Immunohistochemistry demonstrated extensive distribution of CD93 expression mainly in cell membranes in the cerebral cortex. After lipopolysaccharide stimulation, CD93 expression increased and then reduced, with distinct staining in the cytoplasm and nucleus. Double immunofluorescence staining in cerebral cortex of normal rats showed that CD93 and GIPC widely expressed in resting microglia and neurons. CD93 was mainly expressed in microglial and neuronal cell membranes, while GIPC was expressed in both cell membrane and cytoplasm. In the cerebral cortex at 9 hours after model establishment, CD93-immunoreactive signal diminished in microglial membrane, with cytoplasmic translocation and aggregation detected. GIPC localization was unaltered in neurons and microglia. These results are the first to demonstrate CD93 participation in pathophysiological processes of central nervous system inflammation.
Keywords: CD93; GIPC; NSFC grants; brain inflammation model; central nervous system; expression and localization; inducible nitric oxide synthase; intracerebroventricular injection; lipopolysaccharide; microglia; nerve regeneration; neural regeneration; neurons; rats.