Interleukin-19 Promotes Retinal Neovascularization in a Mouse Model of Oxygen-Induced Retinopathy.

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  • Additional Information
    • Source:
      Publisher: Association For Research In Vision And Ophthalmology (Arvo) Country of Publication: United States NLM ID: 7703701 Publication Model: Print Cited Medium: Internet ISSN: 1552-5783 (Electronic) Linking ISSN: 01460404 NLM ISO Abbreviation: Invest Ophthalmol Vis Sci Subsets: MEDLINE
    • Publication Information:
      Publication: Brookline Ma : Association For Research In Vision And Ophthalmology (Arvo)
      Original Publication: St. Louis, Mosby.
    • Subject Terms:
      Retinal Diseases*/metabolism ; Retinal Neovascularization*/metabolism; Animals ; Animals, Newborn ; Disease Models, Animal ; Endothelial Cells/metabolism ; Humans ; Interleukins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Oxygen/metabolism ; Oxygen/toxicity ; Vascular Endothelial Growth Factor A/metabolism
    • Abstract:
      Purpose: Retinal neovascularization is a major cause of blindness. This study aimed to investigate the effects of IL-19 and the underlying mechanisms in a mouse model of oxygen-induced retinopathy (OIR).
      Methods: C57BL/6J wild-type mice and IL-19 knockout (KO) mice were used to establish an OIR mouse model. Bone marrow-derived macrophages (BMDMs) with or without recombinant IL-19 (rIL-19) stimulation were injected intravitreally. Reverse transcription-quantitative polymerase chain reaction was used to determine the mRNA expressions. ELISA and western blotting were performed to assess the protein levels. Immunofluorescence staining was applied to assess retinal neovascularization. Human retinal endothelial cells (HRECs) stimulated with rIL-19 were cultured to evaluate the effects on cell proliferation and migration.
      Results: The level of IL-19 was significantly elevated at postnatal day 17 in OIR retinas. Both the avascular areas and pathological neovascular tufts were significantly increased in rIL-19-treated OIR retinas and suppressed in IL-19 KO retinas. IL-19 KO mice suppressed expression of ARG1, VEGFA, and pSTAT3. Moreover, BMDMs stimulated by rIL-19 enhanced that expression and suppressed the expression of inducible nitric oxide synthase (iNOS). The proliferation and migration of HRECs were significantly augmented by rIL-19. In addition, intravitreal injection of BMDMs stimulated by rIL-19 enhanced retinal neovascularization.
      Conclusions: These findings suggest that IL-19 enhances pathological neovascularization through a direct effect on microvascular endothelial cells and the promotion of M2 macrophage polarization. The inhibition of IL-19 may be a potential treatment for retinal neovascularization.
    • Comments:
      Erratum in: Invest Ophthalmol Vis Sci. 2022 Aug 2;63(9):23. (PMID: 35994253)
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    • Accession Number:
      0 (Interleukins)
      0 (Vascular Endothelial Growth Factor A)
      S88TT14065 (Oxygen)
    • Publication Date:
      Date Created: 20220711 Date Completed: 20220713 Latest Revision: 20220822
    • Publication Date:
      20240829
    • Accession Number:
      PMC9284469
    • Accession Number:
      10.1167/iovs.63.8.9
    • Accession Number:
      35816041