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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Antigens, CD, Cell Adhesion Molecules, Disease Models, Animal, Hyperoxia, Mice, Mice, Inbred C57BL, Oxygen, Retinal Neovascularization, Retinal Vessels, Retinopathy of Prematurity.
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Does cEACAM1 confer resistance toward oxygen-induced vessel damage in a mouse model of retinopathy of prematurity? Context: To determine a functional role for the carcinoembryonic antigen-related cell-adhesion molecule 1 (CEACAM1) in retinal neovascularization in a mouse model of oxygen-induced retinopathy (OIR). In a 21/75/21% OIR mouse model, retinal neovascularization was compared in wild-type and CEACAM1-deficient mice. Animals were housed under normoxic conditions until postnatal day 7, followed by exposure to 75% oxygen for 5 days, and further housing under normoxic conditions. Retinal vascular anatomy, vaso-obliteration, neovascularization, and tuft formation were characterized and quantified in retinal flat-mounts from untreated mice and from experimental mice during and at different time points after exposure to high oxygen levels. The vascular network was stained with fluorescently labeled isolectin B4. Mice deficient in CEACAM1 did not present any apparent abnormalities in their postnatal retinal vascular development under normoxic housing conditions. However, after hyperoxia and under relative hypoxic conditions, retinal neovascularization and tuft formation were aggravated in the mutant. Congruently, revascularization and vessel maturation were delayed in CEACAM1-deficient mice whereas in wild-type mice, tuft regression and vascular remodeling occurred efficiently after exposure to high oxygen levels.
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Our report describes a functional role for CEACAM1 in retinal neovascularization in a mouse model of OIR. This is the first study demonstrating that CEACAM1 enhances vascular remodeling and tuft regression by increasing endothelial resistance to alterations in oxygen tension, thus accelerating vascular recovery after systemic hypoxia. Final Decision: yes