Kraemer F B, Chen Y D, Lopez R D, Reaven G M
J Biol Chem. 1983 Oct 25;258(20):12190-7.
Isolated mouse peritoneal macrophages that had been stimulated with thioglycolate were shown to take up and degrade normal human 125I-very low density lipoproteins (VLDL). Uptake occurred via a specific cell surface receptor which was shown to be 1) temperature-dependent, 2) calcium-dependent, and 3) susceptible to proteolytic digestion. The receptor-mediated uptake and degradation of VLDL markedly stimulated the synthesis and accumulation of triglyceride and cholesteryl ester within macrophages. The degradation of the protein and lipid portions of VLDL occurred within lysosomes. Competition studies showed that the binding site for VLDL was different from the receptor for normal low density lipoproteins or for acetylated low density lipoproteins but that there was cross competition with beta-VLDL. In addition, positive charges appeared to play an important role in the recognition of VLDL by their receptors since polyamines were able to markedly inhibit VLDL binding, degradation, and lipid accumulation while negatively charged compounds were without effects. These studies indicate that 1) stimulated mouse peritoneal macrophages possess specific receptors which recognize normal human VLDL and 2) the receptor-mediated uptake of VLDL results in the accumulation of triglyceride and cholesteryl ester within macrophages.
已证明，用巯基乙酸盐刺激的分离小鼠腹腔巨噬细胞能够摄取并降解正常人的125I-极低密度脂蛋白（VLDL）。摄取通过一种特定的细胞表面受体发生，该受体被证明：1）依赖温度；2）依赖钙；3）易受蛋白水解消化的影响。受体介导的VLDL摄取和降解显著刺激了巨噬细胞内甘油三酯和胆固醇酯的合成与积累。VLDL的蛋白质和脂质部分在溶酶体内发生降解。竞争研究表明，VLDL的结合位点与正常低密度脂蛋白或乙酰化低密度脂蛋白的受体不同，但与β-VLDL存在交叉竞争。此外，正电荷似乎在其受体识别VLDL中起重要作用，因为多胺能够显著抑制VLDL的结合、降解和脂质积累，而带负电荷的化合物则无此作用。这些研究表明：1）受刺激的小鼠腹腔巨噬细胞拥有识别正常人VLDL的特定受体；2）受体介导的VLDL摄取导致巨噬细胞内甘油三酯和胆固醇酯的积累。
