Armstrong D P, White D A
Department of Biochemistry, Queens Medical Centre, Nottingham, England.
Cell Biochem Funct. 1993 Mar;11(1):35-44. doi: 10.1002/cbf.290110105.
The effect of tunicamycin (TM) on the metabolism of acetylated low-density lipoprotein (AcLDL) was examined to determine whether N-linked glycosylation is required for the proper function of the AcLDL pathway. Proteolytic degradation of [125I]-AcLDL was increased twofold in the presence of TM. This did not occur via an increase in total lysosomal enzyme activity or extracellular proteolysis; rather, the rate of uptake of [125I]-AcLDL was increased. The enhanced degradation of AcLDL did not lead to a commensurate increase in the rate of synthesis of cholesteryl oleate. Conversely, the rate of cholesterol esterification was reduced in the presence of TM. The uptake of [125I]-AcLDL was more sensitive to inhibition by chloroquine in TM-treated cells. However, the presence of TM did not affect the ability of chloroquine to inhibit constitutive recycling of AcLDL binding sites. These results suggest that N-linked glycosylation may be involved in the regulation of AcLDL metabolism in J774 cells.
研究了衣霉素(TM)对乙酰化低密度脂蛋白(AcLDL)代谢的影响,以确定N-连接糖基化对于AcLDL途径的正常功能是否必需。在TM存在的情况下,[125I]-AcLDL的蛋白水解降解增加了两倍。这并非通过总溶酶体酶活性或细胞外蛋白水解的增加而发生;相反,[125I]-AcLDL的摄取速率增加。AcLDL降解增强并未导致胆固醇油酸酯合成速率相应增加。相反,在TM存在的情况下,胆固醇酯化速率降低。在经TM处理的细胞中,[125I]-AcLDL的摄取对氯喹抑制更敏感。然而,TM的存在并不影响氯喹抑制AcLDL结合位点组成型循环的能力。这些结果表明,N-连接糖基化可能参与J774细胞中AcLDL代谢的调节。