Seyfried-Williams R, McLaughlin B J, Cooper N G
Exp Cell Res. 1984 Oct;154(2):500-9. doi: 10.1016/0014-4827(84)90174-5.
In the dystrophic pigmented Royal College of Surgeons (RCS) rat, the retinal pigment epithelium (RPE) has a diminished capacity to phagocytose shed photoreceptor outer segments (ROS). An alteration in phagocytic recognition or ligand-receptor interactions between the RPE and ROS's could contribute to this defect. To this end, we have examined whether or not RPE lectin receptors are implicated in phagocytosis in the normal and dystrophic rat RPE by comparing differences in phagocytic uptake of lectin-coated beads. To test this, the following lectins were bound either indirectly to sugar-coated latex beads or directly to activated beads: Concanavalin A (conA), specific for mannose; Ulex europeus (ULEX), specific for fucose; Lens culinaris (LcH), specific for mannose; and wheat germ agglutinin (WGA), specific for N-acetyl glucosamine and sialic acid. The distribution of the lectin binding around beads was visualized and confirmed using lectin-Ferritin conjugates. Lectin-coated beads were fed to normal and dystrophic pigmented RPE tissue explants to determine differences in phagocytic uptake. We found that whether beads were directly or indirectly coated, similar results were obtained, but that there were differences in uptake of two types of lectin-coated beads by dystrophic as compared with normal animals. The dystrophic RPE phagocytosed greater numbers of conA-mannose beads (6.9/cell) than the normal RPE (3.6/cell). LcH-mannose beads were also phagocytosed by dystrophic (2.7/cell) but not by the normal (0/cell). A similar number of ULEX-fucose beads were taken up by dystrophic (3.8/cell) and normal (3.4/cell) RPE and neither took up WGA-N-acetyl glucosamine beads (0/cell). These results showing that the dystrophic RPE takes up greater numbers of conA and LcH-coated beads than the normal RPE suggest that a ligand-receptor interaction involving mannose may contribute to this difference in phagocytic uptake.
在营养不良性色素沉着的皇家外科学院(RCS)大鼠中,视网膜色素上皮(RPE)吞噬脱落的光感受器外段(ROS)的能力减弱。RPE与ROS之间吞噬识别或配体 - 受体相互作用的改变可能导致这种缺陷。为此,我们通过比较凝集素包被珠子的吞噬摄取差异,研究了RPE凝集素受体是否参与正常和营养不良大鼠RPE的吞噬作用。为了验证这一点,将以下凝集素间接结合到糖包被的乳胶珠上或直接结合到活化的珠子上:对甘露糖具有特异性的刀豆球蛋白A(conA);对岩藻糖具有特异性的欧洲荆豆(ULEX);对甘露糖具有特异性的扁豆凝集素(LcH);以及对N - 乙酰葡糖胺和唾液酸具有特异性的麦胚凝集素(WGA)。使用凝集素 - 铁蛋白缀合物可视化并确认珠子周围凝集素结合的分布。将凝集素包被的珠子喂给正常和营养不良性色素沉着的RPE组织外植体,以确定吞噬摄取的差异。我们发现,无论珠子是直接还是间接包被,都得到了相似的结果,但与正常动物相比,营养不良动物对两种类型凝集素包被珠子的摄取存在差异。营养不良的RPE吞噬的conA - 甘露糖珠子数量(6.9个/细胞)比正常RPE(3.6个/细胞)更多。LcH - 甘露糖珠子也被营养不良的RPE吞噬(2.7个/细胞),但正常RPE不吞噬(0个/细胞)。营养不良的RPE(3.8个/细胞)和正常RPE(3.4个/细胞)摄取的ULEX - 岩藻糖珠子数量相似,两者都不摄取WGA - N - 乙酰葡糖胺珠子(0个/细胞)。这些结果表明,与正常RPE相比,营养不良的RPE摄取更多的conA和LcH包被珠子,这表明涉及甘露糖的配体 - 受体相互作用可能导致吞噬摄取的这种差异。