Shiraki K, Burns M S
Curr Eye Res. 1986 Sep;5(9):683-95. doi: 10.3109/02713688609015136.
Rat urethane retinopathy produces sequential and progressive loss of the photoreceptor cells, proceeding from the posterior to the peripheral retina. The inner retina, the retinal pigment epithelium and the choriocapillaris are spared. After loss of the photoreceptor cells, a vasculopathy develops which includes progressive retinal capillary loss and formation of coil-like tufts of retinal vessels which are embedded in the retinal pigment epithelium. Some of the retinal vessels within the retinal pigment epithelium have changed their phenotype from continuous to fenestrated endothelial cells. To elucidate whether DNA synthesis was necessary for formation of the coil-like vessel tuft formation, an autoradiographic study was performed. At 12, 14, 16 and 20 weeks of age, times during which the vasculopathy is known to be forming, urethane and control rats were injected with 3 successive doses of methyl-3H-thymidine. Autoradiography of trypsin-digested retinal vessel preparations was compared with histological sections of the paired eye. The frequency of tritium labelled endothelial cells was much higher in the urethane rats than control animals, and were predominantly in the posterior pole, rather than the periphery. Labelled endothelial cells tended to be associated with, or near, the coil-like vessel tufts. Capillary dropout was observed in urethane, but not control animals. Frequently, adjacent endothelial cells were labelled, suggestive of mitosis. The occurrence of thymidine uptake and a change in phenotype of the endothelial cells leads us to suggest that new cell synthesis, or neovascularization, has occurred in these vessels. Since the retina is less than half the normal thickness and the choriocapillaris is intact, it appears unlikely that ischemia is responsible for inducing these pathological responses. We suggest that the retinal pigment epithelial cell is responsible for the increase in DNA synthesis and change in phenotype of the retinal endothelial cell.
大鼠氨基甲酸乙酯视网膜病变会导致光感受器细胞依次进行性丧失，从视网膜后部向周边发展。视网膜内层、视网膜色素上皮和脉络膜毛细血管不受影响。光感受器细胞丧失后，会出现一种血管病变，包括视网膜毛细血管逐渐丧失以及形成嵌入视网膜色素上皮的盘绕状视网膜血管簇。视网膜色素上皮内的一些视网膜血管内皮细胞表型已从连续性变为有窗孔型。为了阐明DNA合成对于盘绕状血管簇形成是否必要，进行了一项放射自显影研究。在12、14、16和20周龄时（已知血管病变正在形成的时期），给氨基甲酸乙酯处理的大鼠和对照大鼠连续注射3剂甲基 - 3H - 胸腺嘧啶核苷。将胰蛋白酶消化的视网膜血管制剂的放射自显影与对侧眼的组织学切片进行比较。氨基甲酸乙酯处理的大鼠中氚标记的内皮细胞频率比对照动物高得多，且主要位于后极，而非周边。标记的内皮细胞倾向于与盘绕状血管簇相关或靠近它们。在氨基甲酸乙酯处理的大鼠中观察到毛细血管缺失，而对照动物中未观察到。相邻内皮细胞经常被标记，提示有丝分裂。胸腺嘧啶核苷摄取的发生以及内皮细胞表型的改变使我们认为这些血管中发生了新细胞合成或新生血管形成。由于视网膜厚度不到正常厚度的一半且脉络膜毛细血管完好无损，缺血似乎不太可能是诱导这些病理反应的原因。我们认为视网膜色素上皮细胞是视网膜内皮细胞DNA合成增加和表型改变的原因。
