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A.J. Franklin, T.L. Jetton, E.C. Kohn; CAI Appears to Provide Neuroprotection in Mouse Model of Ischemia Induced Retinal Neovascularization . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2926.
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Purpose: To determine if an anti-angiogenic molecule, Carboxyamido-triazole (CAI), exerts a neuroprotective effect in a mouse model of ischemic retinopathy. Methods: Neonatal C57BL/6J mice were subjected to 75-85% oxygen from postnatal day 7 through 12 (PND 7 - 12), and then oxygen concentration was abruptly decreased to 21%, room air. For Group A animals, CAI 2 mg/kg or vehicle control (PEG-400) was given daily on PND 14 - 16, and mice were then sacrificed on PND-17, to characterize whether CAI could inhibit formation of neovascularization. For Group B animals, CAI 2 mg/kg or vehicle control (PEG-400) was given daily on PND 17 - 19, and mice were then sacrificed on PND-20, to characterize whether CAI could affect regression of already formed neovascular fronds. Eyes were enucleated, fixed and subject to light microscopy. Immunohistochemistry with various cell survival markers were performed on both vehicle control and CAI-treated animals in Groups A and B. Results: CAI treatment was associated with a significant upregulation of bcl-2 immunoreactivity in the inner plexiform layer (IPL) for both Groups A and B. In addition, nuclei in the inner nuclear (INL) appeared pyknotic for the vehicle control animals, whereas the INL appeared relatively normal in CAI-treated animals in both Group A and B. Conclusions: In this ischemia induced model of retinal neovascularization, CAI not only is an effective angiogenic inhibitor, but this molecule also produces either a direct or indirect neuroprotective effect upon inner retinal neurons.
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