Wang S P, Feng Z C, Wu W S, Wang C B, Jiang W G, Xu K
J Tongji Med Univ. 1989;9(2):125-8, 124.
Triglyceride was accumulated saturably in cultivated human fibroblasts exposed to increasing concentration of normal very low density lipoprotein (N-VLDL). Characterization of binding and degradation of 125I-N-VLDL by the cells indicated a direct uptake of intact N-VLDL particles via the cell surface receptor. Competition of unlabelled N-VLDL and LDL with 125I-N-VLDL in fibroblasts suggested that LDL receptor may be involved in this process. An unsaturable triglyceride accumulation in fibroblast induced by macrophage-conditioned medium containing N-VLDL was also observed. Intracellular triglyceride content, in this case, is linearly correlated with the concentration of N-VLDL in the medium and results mainly from re-esterification of fatty acid produced by hydrolysis of VLDL-triglyceride by lipoprotein lipase of macrophage.
在暴露于浓度不断增加的正常极低密度脂蛋白(N-VLDL)的培养人成纤维细胞中,甘油三酯呈饱和性蓄积。细胞对¹²⁵I-N-VLDL的结合和降解特性表明,完整的N-VLDL颗粒可通过细胞表面受体直接摄取。成纤维细胞中未标记的N-VLDL和低密度脂蛋白(LDL)与¹²⁵I-N-VLDL的竞争表明,LDL受体可能参与了这一过程。还观察到含有N-VLDL的巨噬细胞条件培养基诱导成纤维细胞中出现不可饱和的甘油三酯蓄积。在这种情况下,细胞内甘油三酯含量与培养基中N-VLDL的浓度呈线性相关,主要是由巨噬细胞脂蛋白脂肪酶水解VLDL-甘油三酯产生的脂肪酸再酯化所致。