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Masayuki Nukada, Tomoaki Murakami, Satoshi Morooka, Ken Ogino, Nagahisa Yoshimura; Annexin V Suppresses Pathological Retinal Angiogenesis And Disrupts Blood-retinal Barrier. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3123.
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Annexin V is shown to be expressed in perivascular cells, although the effects on retinal vascular endothleial cells remain ill-defined. We here investigated how annexin V influences retinal angiogenesis and vascular permeability in the retina.
In order to evaluate the effects on physiological retinal vascular development, Annexin V (1nM) was intraperitoneally injected into C57BL6/J mice on postnatal 2 days (P2), and the eyes were isolated and fixed on P4. The radius of vascularized area (the length between the center of the optic nerve and the edge of leading vessels) was measured. We further evaluated oxygen-induced retinopathy model for analysis of pathological angiogenesis. After the intravitreal injection of annexin V, the area of neovascular tufts was quantified on P17. Modified Miles assay was applied to estimate the effect of annexin V on vascular permeability. 24 hours after the intravitreal administration of annexin V (4nM), Evans Blue was intravenously injected, and the amount of dye extravasated into retinal parenchyma was measured in Sprague-Dawley (SD) rats.
The radius of vascularized area of the retina treated with Annexin V did not show significant difference with that treated with vehicle (881.4±176.3µm vs. 993.1±189.8µm, p=0.12). Meanwhile, the area of neovascular tufts were significantly decreased in retinas administrated with annexin V (1nM) than in those treated with PBS in oxygen-induced retinopathy model (p<0.05), although the avascular area was not different between them (p=n.s). It suggests that annexin V suppressed pathological angiogenesis, but not vascular repair. Additionally, Evans Blue extravasated into retinal parenchyma was increased in the retina treated with intravitreal injection of annexin V (p<0.01).
These data suggest that annexin V suppressed pathological, but not physiological retinal angiogenesis, and induced hyperpermeability in the retinal vasculature.
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