Modulation of inflammatory responses in mouse models of pericyte-depletion retinopathy
A major feature of diabetic retinopathy is pericyte loss. Here, we have utilzed a model of pericyte depletion retinopathy that recapitulates key features of human diabetic retinopathy to study the cellular and molecular components of the diease and response to immunomodulation with minocylcine. Pericyte depletion was achieved via injection of a rat anti-mouse PDGFRB mAb at Postnatal day 1 (P1) in C57BL6/J WT mice. Treatment with minocyline begaun at P5, daily until P27, and retinas analysed from P28 mice. Transcriptomic analyses identifies signature pathways in pericyt-depletion retinopathy and response to minoccyline Overall design: RNAseq-profiling of 4-weeks (p28) old retina transcriptome of WT mice (C56BL6/J) following treatment with IgG or a rat anti-mouse PDGFRB mAb at postnatal day 1 with and withut daily treatment with minocyline (P5-p27) at a dose of 45mg/kg bw