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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE276207 | GEO | 2025/02/17

REPOSITORIES: GEO

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Project description:The hallmark of IgA nephropathy (IgAN) is gross hematuria (GH) coinciding with or immediately following an upper respiratory or gastrointestinal tract infection and can represent the disease triggering event. Therefore, a whole genomic screening of IgAN patients during the GH was done to clarify the link between mucosal encountered antigens and the occurrence of glomerular hematuria. The modulated genes during GH show a clear involvement of the interferon signalling, antigen presenting pathway, and the immuno-proteasome. The gene characterizing cytotoxic effector lymphocytes (CX3CR1) implicated in vascular endothelial damage, was found up-regulated at both mRNA and protein level. In vitro antigenic stimulation of PBMCs on an independent set of IgAN patients and healthy blood donors (HBS) demonstrated that patients upregulate specifically CX3CR1 in an enhanced and dose dependant manner, while an expected down-regulation occurred in HBD. This enhanced activation occurred in both patients characterized by recurrent GH and by permanent microscopic hematuria (MH). We then analyzed glomerular fractalkine (FKN) expression, since this ligand is involved in the vascular gateway for CX3CR1+ cells towards the inflamed tissues. A significantly higher FKN expression on the capillary vessels and podocytes was found in recurrent GH patients compared to permanent MH, suggesting a predisposition for cytotoxic cell extravasation in recurrent GH patients. Taken together, our findings demonstrate, for the first time, a defect in antigen handling in PBMCs of IgAN patients with a specific up-regulation of CX3CR1. Furthermore, the constitutive up regulation of glomerular FKN, suggests an involvement of the CX3CR1-FKN axis in the exacerbation of GH. Gene expression profile comparison 3 IgAN patients at two different clinical time points, the first sample during the gross hematuria episode and the second during the remission phase of the disease characterized by microscopic hematuria

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

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