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.

视网膜胶质细胞向视网膜外的迁移是一个重要的 许多增生性视网膜病的病理生理学方面，包括 增殖性玻璃体视网膜病变（PVR）和纤维血管视网膜病变， 糖尿病性玻璃体视网膜病变、早产儿视网膜病变和创伤性视网膜病变 玻璃体视网膜病变 最吸引人的假设是 在这些病理中作为最终共同途径的神经胶质增生是神经胶质细胞的分泌或 视网膜释放蛋白质，刺激迁移， 视网膜胶质细胞在各种生理和病理条件下的生长 压力 我们从正常牛视网膜中纯化了一种蛋白质， 在各种神经胶质细胞中引发迁移反应，我们将其命名为 视网膜趋化蛋白 这里提出的研究将提供一个准确的确定 视网膜趋化蛋白的物理性质，并测量其 对细胞外基质迁移、增殖和沉积的影响 基质中的视网膜胶质细胞。 眼细胞的体外研究将 确定调节释放或分泌的生理参数 这种蛋白质。 这项工作将进一步确定视网膜的作用， 使用猫动物模型的视网膜脱离中的趋化蛋白。 最后，玻璃体吸出物和细胞膜在 玻璃体切除术将用于确定这种相同的蛋白质在人类中的作用。 涉及神经胶质迁移和增殖的病理学。 这项工作将提供一个基本的了解视网膜的反应， 损伤 由于增生的神经胶质细胞直接干扰视网膜的 再附着，并可以提供一种结构，在其上其他眼细胞 类型可以连接和分裂，这些结果应该导致增强的 有能力设计新的治疗方法， 疾病