RNA-seq analysis reveals differentially expressed inflammatory chemokines in a rat retinal degeneration model induced by sodium iodate

Abstract

Objective Retinal degeneration (RD) is a group of serious blinding eye diseases characterized by photoreceptor cell apoptosis and progressive degeneration of retinal neurons. However, the underlying mechanism of its pathogenesis remains unclear. Methods In this study, retinal tissues from sodium iodate (NaIO3)-induced RD and control rats were collected for transcriptome analysis using RNA-sequencing (RNA-seq). Analysis of white blood cell-related parameters was conducted in patients with retinitis pigmentosa (RP) and age-related cataract (ARC) patients. Results In total, 334 mRNAs, 77 long non-coding RNAs (lncRNAs), and 20 other RNA types were identified as differentially expressed in the retinas of NaIO3-induced RD rats. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses showed that differentially expressed mRNAs were mainly enriched in signaling pathways related to immune inflammation. Moreover, we found that the neutrophil-to-lymphocyte ratio was significantly higher in RP patients than in ARC patients. Conclusion Overall, this study suggests that multiple chemokines participating in systemic inflammation may contribute to RD pathogenesis.

Oxidative Stress and Lipid Accumulation Augments Cell Death in LDLR-Deficient RPE Cells and Ldlr−/− Mice

“…A number of preclinical investigations have shown that oxidative stress stimulates the initiation and amplification of inflammatory pathways in a wide range of cell types in the retina and choroid [47][48][49]. Recent research has also shown that the NaIO 3 model modulates soluble immune proteins, complement proteins, and cytokines/chemokines in a time-dependent manner, supporting the idea that this model could be used to mimic retinal inflammatory sequences [41,50]. Ldlr −/− mice fed with high-fat diet for 12 weeks had increased oxidized lipids and inflammatory markers and caused pulmonary hypertension [51], suggesting a role for LDLR and oxidized lipids in the initiation of diseases.…”