REGULATION OF VESSEL REGRESSION IN ISCHEMIC RETINOPATHY

缺血性视网膜病变中血管退化的调节

• 批准号: 7715979
• 负责人: Charles T Roberts
• 金额: $ 1.11万
• 依托单位: OREGON HEALTH & SCIENCE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-05-01 至 2009-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7715979
• 关键词: Apoptosis; Blindness; Blood Vessels; Cessation of life; Class; Computer Retrieval of Information on Scientific Projects Database; Disease; Disease regression; Endothelial Cells; Eph Family Receptors; EphA1 Receptor; Funding; Goals; Grant; Institution; Lead; Life; Ligands; Microglia; Mus; Pathologic Neovascularization; Regulation; Research; Research Personnel; Resources; Retinal; Retinal Diseases; Retinal Neovascularization; Retinopathy of Prematurity; Role; Signaling Molecule; Source; Testing; United States National Institutes of Health; antiangiogenesis therapy; macrophage; mouse model; neovascularization; novel; novel therapeutics; receptor; therapeutic angiogenesis

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Retinopathy of prematurity (ROP) is a disorder of pathological retinal neovascularization, which can result in life-long blindness. The long-term goal of this project is to acquire a better understanding of the mechanisms surrounding retinal neovascularization in order to develop anti-angiogenesis therapies. We hypothesize that directly modulating pre-retinal endothelial cell (EC) apoptosis will be an efficient anti-angiogenic approach despite the multiple factors that can promote pathological angiogenesis. A novel class of signaling molecules, the ephrin/Eph receptors are also candidate molecules to regulate EC neovascularization and apoptosis. In order to test our hypothesis and identify mechanisms that are responsible for vascular tuft apoptosis, we propose the following specific Aims: 1) Identify specific death receptors that lead to EC apoptosis and promote tuft regression, specifically determine if direct activation of Fas will induce vessel regression; 2) Identify the contribution of microglia and macrophages to the regression of retinal neovascularization and their ability to induce apoptosis through the use of genetically altered mice; and 3) Further understand the role of ephrin/Eph receptors in retinal neovascularization by developing new therapeutic approaches to induce vessel regression, using soluble ligands to modulate the ephrin/Eph receptors in the mouse model of OIR.

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