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

有研究认为，视网膜循环障碍与青光眼的发生和发展有关。本研究表明，在视网膜缺血再灌注和玻璃体内注射NMDA诱导的大鼠视网膜变性模型中，视网膜血管在结构和功能上受到损伤。在这些模型中，视网膜层的变化仅限于内视网膜，表现为视网膜神经节细胞的丢失和内网状层的变薄。因此，内视网膜内呈现的神经元细胞可能通过生成/释放血管细胞的生长因子和营养因子来维持血管结构。例如，在本研究中，我们发现大鼠视网膜视网膜神经节细胞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丧失可能无法提供足够量的VEGF来维持血管结构和功能。因此，神经元细胞损伤可能通过减少视网膜神经元的血液供应而成为视网膜损伤进展的另一个原因。保护视网膜血管的结构和功能是预防青光眼发展的新策略。

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.