BIOCHEMICAL MODULATION OF RETINAL GLIOSIS

视网膜胶质细胞增生的生化调节

• 批准号: 3262655
• 负责人: Leonard Martin Hjelmeland
• 金额: $ 21.2万
• 依托单位: UNIVERSITY OF CALIFORNIA AT DAVIS
• 依托单位国家: 美国
• 财政年份: 1986
• 资助国家: 美国
• 起止时间: 1986-07-01 至 1991-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3262655
• 关键词: basement membrane; cell migration; chromatography; disease /disorder model; electrofocusing; extracellular matrix; human tissue; microglia; monoclonal antibody; radiotracer; retina; retina detachment; retina disorder; retinal pigment epithelium; secretion; tissue /cell culture; vitrectomy; vitreous body

The migration of retinal glial cells to extra-retinal sites is an important aspect of the pathophysiology of many proliferative retinopathies including proliferative vitreoretinopathy (PVR), and fibovascular-retinopathies such as diabetic vitreoretinopathy, retinopathy of prematurity, and traumatic vitreoretinopathy. The most attractive hypothesis which accounts for gliosis as a final common pathway in these pathologies is the secretion or release of a protein by the retina which stimulates the migration and growth of retinal glia under a variety of physiological and pathological stresses. We have purified a protein from normal bovine retina which elicites a migratory response in various neural glia, which we have named the retinal chemotactic protein. The research proposed here will provide an accurate determination of the physical properties of the retinal chemotactic protein and measure its effect on the migration, proliferation, and deposition of extracellular matrix by retinal glia in vitro. Studies of ocular cells in vitro will determine the physiological parameters regulating the release or secretion of this protein. This work will further establish the role of the retinal chemotactic protein in retinal detachment using the cat animal model. Finally, vitreous aspirates and celullar membranes removed during vitrectomy will be used to establish the role of this same protein in human pathologies involving glial migration and proliferation. This work will provide a basic understanding of the retina's response to injury. Since proliferated glial cells directly interfere with retinal reattachment, and may provide a structure upon which other ocular cell types may attach and divide, these results should lead to an enhanced ability to design new forms of treatment for these devastating retinal diseases.

视网膜神经胶质细胞向视网膜外部位的迁移是重要的 许多增殖性视网膜病的病理生理学方面 增生性玻璃体病（PVR）和外观性肿瘤病这样 作为糖尿病性玻璃体病，早产性视网膜病变和创伤性 玻璃体病。 说明的最有吸引力的假设 神经胶质为这些病理中的最终公共途径是分泌或 通过视网膜释放蛋白质，刺激迁移和 视网膜神经胶质在多种生理和病理下的生长 压力。 我们已经从正常牛视网膜中纯化了一种蛋白质 精神属于各种神经神经胶质的迁移反应，我们已经命名了 视网膜趋化蛋白。 这里提出的研究将提供准确的确定 视网膜趋化蛋白的物理特性并测量其 对细胞外迁移，增殖和沉积的影响 体外视网膜胶质的基质。 在体外研究眼细胞会 确定调节释放或分泌的生理参数 该蛋白质。 这项工作将进一步确定视网膜的作用 使用CAT动物模型的视网膜脱离中的趋化蛋白。 最后，在 玻璃体切除术将用于确定这种相同蛋白在人类中的作用 涉及神经胶质迁移和增殖的病理。 这项工作将提供对视网膜回应的基本理解 受伤。 由于增殖的神经胶质细胞直接与视网膜干扰 重新介绍，可以提供其他眼部细胞的结构 类型可能附着和分裂，这些结果应导致增强 能够为这些破坏性的视网膜设计新形式的治疗形式 疾病。