Burns M S, Tyler N K
Department of Ophthalmology, School of Medicine, University of California, Davis.
Curr Eye Res. 1990 Nov;9(11):1061-75. doi: 10.3109/02713689008997580.
Photoreceptor cell degeneration in rodents from a variety of causes results in neovascularization of the retinal pigment epithelium as a late stage phenomenon. Even though the vessels within the pigment epithelium arise from the retinal circulation, they can manifest the choroidal endothelial cell phenotype of fenestrated endothelial cells. In order to study the detailed cellular events which result in incorporation of retinal vessels within the retinal pigment epithelium, a morphological and morphometric analysis of the RPE and vasculature was performed in rats. Urethane, given subcutaneously to newborn rats, results in a photoreceptor degeneration but does not affect the RPE, choroid or inner retinal layers. Retinas were studied from rats of 8 to 24 weeks of age, the time period when vascularization of the RPE occurs. Loss of retinal vessels is first seen at 12 weeks, primarily in substantial dropout of vessel profiles in the outer plexiform layer (OPL) vessel bed. There is a gradient of loss from the OPL bed to the nerve fiber layer (NFL) bed and from the central to peripheral region. Total vessel density of the experimental retinas is greater than controls at 8 and 12 weeks. This occurs because there is marked loss of retinal thickness, due to photoreceptor degeneration, without a comparable loss of vessel profiles. The total retinal vessel density decreases from 8 to 20 weeks, and appears to stabilize at 20 and 24 weeks. Analysis of the separate vessel beds shows that this apparent stabilization is due to continued loss of vessels within the sensory retina, and increased presence of vascular profiles within the RPE. Total absence of the photoreceptor cell is necessary for incorporation of vessels within the RPE. Since new vessel profiles develop in the RPE but not the adjacent sensory retina, we speculate that the RPE may stimulate neovascularization of the RPE. A model of the cellular events leading to RPE neovascularization is proposed.
多种原因导致的啮齿动物光感受器细胞变性会在晚期引发视网膜色素上皮的新生血管形成。尽管色素上皮内的血管起源于视网膜循环，但它们可表现出有窗孔内皮细胞的脉络膜内皮细胞表型。为了研究导致视网膜血管纳入视网膜色素上皮的详细细胞事件，对大鼠的视网膜色素上皮和脉管系统进行了形态学和形态计量学分析。给新生大鼠皮下注射乌拉坦会导致光感受器变性，但不影响视网膜色素上皮、脉络膜或视网膜内层。研究了8至24周龄大鼠的视网膜，这是视网膜色素上皮发生血管化的时间段。视网膜血管的丧失首先在12周时出现，主要表现为外丛状层（OPL）血管床中血管轮廓的大量缺失。从OPL床到神经纤维层（NFL）床以及从中央到周边区域存在丧失梯度。实验性视网膜的总血管密度在8周和12周时高于对照组。这是因为由于光感受器变性，视网膜厚度明显减少，而血管轮廓没有相应减少。总视网膜血管密度从8周降至20周，并在20周和24周时似乎稳定下来。对不同血管床的分析表明，这种明显的稳定是由于感觉视网膜内血管的持续丧失以及视网膜色素上皮内血管轮廓的增加。视网膜色素上皮内血管的纳入需要光感受器细胞完全缺失。由于新的血管轮廓在视网膜色素上皮而非相邻的感觉视网膜中形成，我们推测视网膜色素上皮可能刺激其自身的新生血管形成。提出了一个导致视网膜色素上皮新生血管形成的细胞事件模型。
