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Molecular basis for the homeostatic mechanisms that maintain retinal blood vessels and the application for development of anti-glaucoma drugs

维持视网膜血管稳态机制的分子基础及其在抗青光眼药物开发中的应用

基本信息

批准号：
20590090
负责人：
NAKAHARA Tsutomu
金额：
$ 3万
依托单位：
Kitasato University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2008
资助国家：
日本
起止时间：
2008 至 2010
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20590090/
关键词：
薬理学血管生物学微小循環

项目摘要

It has been suggested that an impairment of retinal circulation contributes to the onset and progression of glaucoma. This study demonstrates that retinal blood vessels are damaged structurally and functionally in rat models of retinal degeneration induced by the retinal ischemia-reperfusion and by an intravitreal injection of NMDA. In these models, changes in retinal layer are limited in the inner retina as demonstrated by loss of retinal ganglion cells and thinning of inner plexiform layer. Therefore, it is likely that neuronal cells presented in the inner retina play a role in maintaining the vascular structure through production/release of growth factors and trophic factors for vascular cells. For example, in this study, we found that retinal ganglion cells express vascular endothelial growth factor (VEGF) in rat retina. The loss of retinal ganglion cells that are one of sources of VEGF in the retina may fail to provide sufficient amounts of VEGF for maintaining the vascular structure and function. Thus, neuronal cell damage may be an additional cause of progression of the retinal damage by reducing blood supply to retinal neurons. The protection of retinal vascular structure and function would be a novel strategy for preventing progression of glaucoma.

已经提出视网膜循环的损伤有助于青光眼的发作和进展。本研究表明，视网膜缺血再灌注和玻璃体内注射NMDA诱导的视网膜变性大鼠模型中，视网膜血管结构和功能受损。在这些模型中，视网膜层的变化局限于内层视网膜，如通过视网膜神经节细胞的损失和内网状层的变薄所证明的。因此，可能存在于视网膜内层的神经元细胞通过产生/释放血管细胞的生长因子和营养因子而在维持血管结构中起作用。例如，在本研究中，我们发现视网膜神经节细胞在大鼠视网膜中表达血管内皮生长因子（VEGF）。作为视网膜中VEGF来源之一的视网膜神经节细胞的损失可能无法提供足够量的VEGF用于维持血管结构和功能。因此，神经元细胞损伤可能是通过减少对视网膜神经元的血液供应而导致视网膜损伤进展的另一个原因。保护视网膜血管结构和功能将成为预防青光眼进展的新策略。