REGULATION OF FGF EXPRESSION DURING RETINAL DETACHMENT

视网膜神经胶质细胞向视网膜外的迁移是一个重要的 许多增殖性视网膜病变的病理生理学方面，包括 增殖性玻璃体视网膜病变(PVR)以及纤维血管视网膜病变等 如糖尿病玻璃体视网膜病变、早产儿视网膜病变和外伤性 玻璃体视网膜病变。最有吸引力的假设解释了 在这些病理中，胶质细胞增生症是一种最终的共同途径，是分泌或 视网膜释放一种蛋白质，刺激移行和 多种生理和病理条件下视网膜神经胶质细胞的生长 压力。我们已经从正常的牛视网膜中提纯了一种蛋白质 在各种神经胶质细胞中激发一种迁移反应，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及其测定 对细胞外迁移、增殖和沉积的影响 在体外由视网膜神经胶质细胞形成基质。眼球细胞的体外研究将 确定调节释放或分泌的生理参数 这种蛋白质的。这项工作将进一步确立视网膜的作用 利用猫动物模型研究视网膜脱离中的趋化蛋白。 最后，在手术过程中去除玻璃体抽吸物和纤维膜。 玻璃体切割术将被用来确定这种相同的蛋白质在人类中的作用 涉及神经胶质细胞迁移和增殖的病理学。 这项工作将提供对视网膜反应的基本了解 受伤。由于增殖的胶质细胞直接干扰视网膜 并且可以提供一种结构，在该结构上其他眼细胞 类型可以附加和划分，这些结果应该会导致增强 为这些毁灭性的视网膜设计新的治疗形式的能力 疾病。

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.