CX3CR1-Fractalkine Dysregulation Affects Retinal GFAP Expression, Inflammatory Gene Induction, and LPS Response in a Mouse Model of Hypoxic Retinopathy

Diabetic retinopathy (DR) causes vision loss due to sustained inflammation and vascular dam-age. The vascular damage is characterized fibrinogen leakage, angiogenesis, and hypoxia exac-erbating retinal damage. Neuronal regulation of microglia via the CX3CL1 (FKN)-CX3CR1 pathway also play a significant role in retinal pathology; here defects in the FKN-CX3CR1 pathway exacerbate inflammation, vascular damage and vision impairment. However, the con-tribution of hypoxic astrocytes to the pathological process of DR is unclear. We tested how microglia dysregulation affected the retinal transcriptome under conditions of short duration (7-days) hypoxia-induced retinopathy. Age matched wild type (WT) and CX3CR1 knockout (CX3CR1-KO, CX3KO) mouse were housed under control (22.1% oxygen) or hypoxic (7.5% oxygen) conditions.