Philp N J, Nachmias V T, Lee D, Stramm L, Buzdygon B
Department of Anatomy, School of Medicine, University of Pennsylvania, Philadelphia 19104.
Exp Eye Res. 1988 Jan;46(1):21-8. doi: 10.1016/s0014-4835(88)80089-7.
It has been suggested that rhodopsin may have a direct role in the attachment of shed rod outer segments (ROS) to retinal pigmented epithelial (RPE) cells initiating the events which lead to engulfment. We isolated the soluble tryptic glycopeptide from rhodopsin (GP-T1) and used it as a probe to test this hypothesis. In phagocytic assays using both cultured chick and cat RPE cells, GP-T1 did not inhibit the phagocytosis of ROS. Additionally, mannose glycoconjugates were not effective inhibitors of phagocytosis. However, glycopeptides released by tryptic digestion of intact ROS did inhibit ROS uptake by the RPE cells. The results suggest that phagocytosis of ROS is not mediated through a simple carbohydrate recognition system and that rhodopsin is not the ligand recognized by RPE cells.
有人提出，视紫红质可能在脱落的视杆外段（ROS）与视网膜色素上皮（RPE）细胞的附着过程中起直接作用，启动导致吞噬的一系列事件。我们从视紫红质中分离出可溶性胰蛋白酶糖肽（GP-T1），并将其用作探针来检验这一假设。在使用培养的鸡和猫RPE细胞的吞噬试验中，GP-T1并未抑制ROS的吞噬作用。此外，甘露糖糖缀合物也不是有效的吞噬抑制剂。然而，完整ROS经胰蛋白酶消化释放的糖肽确实抑制了RPE细胞对ROS的摄取。结果表明，ROS的吞噬作用不是通过简单的碳水化合物识别系统介导的，视紫红质也不是RPE细胞识别的配体。
