system
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, Choroid, Choroidal Neovascularization, Disease Models, Animal, Edema, Electroretinography, Enzyme-Linked Immunosorbent Assay, Fluorescein Angiography, Fundus Oculi, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Microscopy, Confocal, Microscopy, Electron, Ophthalmoscopy, Phenotype, Retinal Pigment Epithelium, Retinal Vessels, Signal Transduction, Tomography, Optical Coherence, Vascular Endothelial Growth Factor A.
user
Is spontaneous CNV in a novel mutant mouse associated with early VEGF-A-driven angiogenesis and late-stage focal edema , neural cell loss , and dysfunction? Context: Characterization of a mouse model of spontaneous choroidal neovascularization (sCNV) and its effect on retinal architecture and function. The sCNV mouse phenotype was characterized by using fundus photography, fluorescein angiography, confocal scanning laser ophthalmoscopy (SLO), optical coherence tomography (OCT), ERG, immunostaining, biochemistry, and electron microscopy. A role for VEGF-A signaling in sCNV was investigated by using neutralizing antibodies and a role for macrophages explored by cell-depletion studies. The sCNV starts between postnatal day 10 and 15 (P10-P15), increasing in number and severity causing RPE disruption and dysfunction. Various morphological methods confirmed the choroidal origin and subretinal position of the angiogenic vessels. At approximately P25, vessels were present in the outer retina with instances of anastomosis of some sCNV lesions with the retinal vasculature. The number of CNV lesions was significantly decreased by systemic blockade of the VEGF-A pathway. Choroidal neovascularization size also was significantly modulated by reducing the number of lesion-associated macrophages. Later stages of sCNV were associated with edema, neuronal loss, and dysfunction.
assistant
The sCNV mouse is a new model for the study of both early and late events associated with choroidal neovascularization. Pharmacological reduction in sCNV with VEGF-A antagonists and an anti-inflammatory strategy suggests the model may be useful for investigating novel targets for treating human ocular neovascular disease. Final Decision: yes