Abstract Title
Effect of Endothelial-Specific FoxO1 Deletion on the Architecture of Adult Retinal Microvessels
Abstract
The retina is a thin, light-sensitive tissue lining the back of the eye and contains complex neuronal-microvessel interactions that mimic the blood-brain barrier (BBB), but is more accessible for observation and quantification. FoxO1, a transcription factor that is potentially implicated in propagating neuroinflammatory disease, has conversely been shown to increase aberrant angiogenesis and lethality when reduced or knocked out during development. It remains uncertain if the same would be true for FoxO1 deletion from mature microvessels of adult mice. Therefore, in order to study the role of FoxO1 in mature microvessels, a mouse model with conditional, endothelial-specific FoxO1 deletion was utilized. Considering the potential for aberrant angiogenesis, a study was initiated to determine the impact of such a deletion on adult retinal microvessels. FoxO1 ablation was completed in adult mice, and after 40 days, the retinas were removed for examination via confocal fluorescence microscopy. Preliminary results suggest that FoxO1-deficient mice exhibit some atypical retinal microvessel architecture compared to control mice. Further studies involving more in-depth morphometric analyses of retinal microvessels, including comparison with other vascular beds and additional controls, will be required to determine the extent and possible consequences of these differences.
Effect of Endothelial-Specific FoxO1 Deletion on the Architecture of Adult Retinal Microvessels
The retina is a thin, light-sensitive tissue lining the back of the eye and contains complex neuronal-microvessel interactions that mimic the blood-brain barrier (BBB), but is more accessible for observation and quantification. FoxO1, a transcription factor that is potentially implicated in propagating neuroinflammatory disease, has conversely been shown to increase aberrant angiogenesis and lethality when reduced or knocked out during development. It remains uncertain if the same would be true for FoxO1 deletion from mature microvessels of adult mice. Therefore, in order to study the role of FoxO1 in mature microvessels, a mouse model with conditional, endothelial-specific FoxO1 deletion was utilized. Considering the potential for aberrant angiogenesis, a study was initiated to determine the impact of such a deletion on adult retinal microvessels. FoxO1 ablation was completed in adult mice, and after 40 days, the retinas were removed for examination via confocal fluorescence microscopy. Preliminary results suggest that FoxO1-deficient mice exhibit some atypical retinal microvessel architecture compared to control mice. Further studies involving more in-depth morphometric analyses of retinal microvessels, including comparison with other vascular beds and additional controls, will be required to determine the extent and possible consequences of these differences.