Irie S, Kishimoto T, Tavassoli M
Veterans Administration Medical Center, Jackson, Mississippi 39216.
J Clin Invest. 1988 Aug;82(2):508-13. doi: 10.1172/JCI113625.
To examine the role of liver endothelium in desialation of transferrin (TF), pulse-chase studies were done by incubation of either 3H (sialic acid labeled)-, or 125I, or 59Fe (protein core labeled)-TF with fractionated liver endothelium. While 125I or 59Fe labels were externalized after initial binding and internalization, a large proportion of 3H label was internalized and remained within the cell. When the supernatant of these experiments was studied by isoelectricfocusing and Ricinus communis agglutinin (RCA120) affinity chromatography, generation of asialotransferrin was noted by both techniques. Incubation of liver endothelium with double-labeled TF (sialic acids with 3H and protein core with 125I or 59Fe) led initially to a concordant uptake of the two labels, which were then dissociated and 3H was retained by the cell. These findings indicate desialation of TF by liver endothelium. The significance of these findings in the pathogenesis of hepatic siderosis is discussed.
为了研究肝内皮细胞在转铁蛋白（TF）去唾液酸化过程中的作用，通过将3H（唾液酸标记）、125I或59Fe（蛋白核心标记）标记的TF与分离的肝内皮细胞孵育进行脉冲追踪实验。虽然125I或59Fe标记在最初结合和内化后被外化，但大部分3H标记被内化并保留在细胞内。当通过等电聚焦和蓖麻凝集素（RCA120）亲和层析研究这些实验的上清液时，两种技术均检测到了去唾液酸转铁蛋白的生成。用双标记TF（3H标记唾液酸，125I或59Fe标记蛋白核心）孵育肝内皮细胞最初导致两种标记物的一致摄取，随后它们解离，3H被细胞保留。这些发现表明肝内皮细胞可使TF去唾液酸化。本文讨论了这些发现在肝铁沉着症发病机制中的意义。
