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J.-H. Chang, D. Kim, K.-Y. Han, D. T. Azar, T. Doetschman; Alkali Burn Model of Diminished Corneal Neovascularization and Lymphangiogenesis in bFGF Knockout Mice. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5708.
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© ARVO (1962-2015); The Authors (2016-present)
To characterize alkali burn-induced corneal angiogenesis and lymphangiogenesis in bFGF knockout mice.
bFGF knockout and wild type mouse corneas were treated with 1N NaOH for 1 minute. Alkali burn wounded WT and bFGF knockout mouse corneas were harvested on days 0, 7 and 14. The wounded WT and bFGF knockout mice corneas were analyzed for the expression of angiogenic and anti-angiogenic factors including VEGF-A, -B, -C, -D, LYVE-1, CD31, F4/80, Gr-1 and VEGF receptor-1, -2 and -3.
Corneal neovascularization was diminished in bFGF knockout mice in comparison to that of WT mouse corneas in the alkali burn models. In the wounded corneas, the level of VEGF receptor-2 and -3 are lower in the bFGF knockout mouse corneas than levels observed in wounded WT corneas. Similarly, diminished levels of macrophage (F4/80) and neutrophil (Gr-1) markers VEGF-A and -C was observed by immunostaining in the alkali burn wounded bFGF knockout mouse corneas.
bFGF knockout mice displayed diminished alkali burn-induced corneal angiogenesis and lymphangiogenesis. This reduction may be mediated in part by a reduction of angiogenic factors and inflammatory cells in the wounded bFGF knockout mouse corneas. Understanding the mechanism and role of bFGF in alkali-burn-induced corneal angiogenesis may lead to therapeutic intervention in preventing corneal trauma/alkali burn wounding and angiogenesis-related disorders.
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