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Related Experiment Video

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Experimental Autoimmune Uveitis: An Intraocular Inflammatory Mouse Model
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Retinal endothelial cell phenotypic modifications during experimental autoimmune uveitis: a transcriptomic approach.

Deborah A Lipski1,2, Vincent Foucart3,4,5, Rémi Dewispelaere3,4

  • 1Ophthalmology Group, IRIBHM (Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire), Université Libre de Bruxelles (ULB), Erasme Campus, Building C, Room C6.117, 808 Route de Lennik, 1070, Brussels, Belgium. dlipski@ulb.ac.be.

BMC Ophthalmology
|March 19, 2020
PubMed
Summary

Investigating gene regulation in experimental autoimmune uveitis (EAU) revealed new candidate genes and pathways involved in blood-retinal barrier (BRB) breakdown. This study highlights novel molecular mechanisms underlying non-infectious posterior uveitis.

Keywords:
Blood-retinal barrierEndothelial cellsInflammationLipocalin 2RNA-SeqTranscriptomeUveitisackr1lrg1serpina3n

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Area of Science:

  • Ophthalmology
  • Immunology
  • Genomics

Background:

  • Blood-retinal barrier (BRB) cells undergo significant phenotypic changes during experimental autoimmune uveitis (EAU).
  • Understanding the mechanisms of BRB breakdown is crucial for non-infectious uveitis research.

Purpose of the Study:

  • To investigate the global gene regulation in total retinal cells and retinal endothelial cells during EAU.
  • To identify novel molecular players in BRB breakdown during non-infectious uveitis.

Main Methods:

  • Retinal endothelial cells were isolated using flow cytometry in Tie2-GFP and wild type C57BL/6 mice.
  • EAU was induced, and gene expression was compared between naïve and EAU mice using RNA-Seq.
  • Protein expression of selected genes was validated via immunofluorescence and flow cytometry.

Main Results:

  • RNA-Seq of total retinal cells showed upregulation of genes related to antigen presentation and T cell activation in EAU.
  • Specific transcriptome analysis identified 82 modulated genes in retinal endothelial cells during EAU.
  • Protein validation confirmed the expression of serpina3n, lcn2, ackr1, lrg1, and lamc3 in inner BRB cells.

Conclusions:

  • The study confirms known pathogenic molecules and identifies new candidate genes implicated in inner BRB breakdown.
  • These findings offer novel insights into the molecular mechanisms of non-infectious posterior uveitis.