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S. Radetzky, N. Kociok, C. Gavranic, B. Kirchhof, A.M. Joussen; Altered Reaction of the Retinal Vasculature to Hypoxia at P14 after Oxygen Treatment in ICAM-1 Deficient Mice . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2919.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: ICAM-1 has been identified as a mediator of inflammatory and VEGF-dependent corneal neovascularization. Furthermore, ICAM-1 has been demonstrated to be involved in leukocyte-mediated endothelial injury in diabetic retinopathy. Here we investigated the role of ICAM-1 in retinal vaso-obliteration and neovascularization. Methods: ICAM-1 deficient mice and their respective wild-type controls were exposed to 70% oxygen from postnatal day 7 (P7) to day 12 (P12) and recovered at room air thereafter. The retinal vasculature was examined on day 14, 17, 20. The retinal vasculature was quantified using a density slicing method evaluating the vasculature after perfusion with FITC-concanavalin A. mRNA levels of VEGF, as well as PDGF were quantitatively analyzed by real-time RT-PCR. Results: ICAM-1 deficient mice and their respective wild-type controls exhibited similar retinal development without oxygen treatment. In contrast, there was a more complete vascularization in ICAM-1 -/- mice compared to the wild-type controls after oxygenation at P17. In all oxygen treated groups VEGF and PDGF mRNA expression was significantly increased compared to age-matched controls. Together with the more complete vascularization, VEGF levels were significantly reduced as well as PDGF in ICAM-1 knockout mice. Conclusions: ICAM-1 deficient mice exhibit an altered ability to control the degree of neovascularization. ICAM-1 deficient mice have a more complete vascularization earlier in the hypoxic phase and thus seem to be less responsive to hypoxia, as determined by a reduced retinal VEGF expression.
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