巨噬细胞极低密度脂蛋白受体的调节作用

Regulation of Very Low Density Lipoprotein Receptor on Mouse Peritoneal Macrophages

本文研究了小鼠腹腔巨噬细胞极低密度脂蛋白(VLDL)受体的调节。用富含甘油三酯(TG)的VLDL与小鼠巨噬细胞预温育后,细胞结合^(125)I-VLDL的最大结合容量(Bmax)比对照细胞只降低5％(1071/1127ng/mg细胞蛋白质),当细胞内TG增加到对照的2.5倍时,细胞摄取及降解^(125)I-VLDL的量分别下降40％和22％;乙酰-低密度脂蛋白(AC-LDL)预温育的细胞结合^(125)I-VLDL的Bmax比对照细胞只降低14％(633/831ng/mg细胞蛋白质),当细胞内胆固醇(Ch)增加到对照的23倍时,细胞摄取及降解^(125)I-VLDL的量只分别下降10％和21％。此后随着细胞内TG或Ch含量的增加,摄取及降解^(125)I-VLDL的量仍保持不变。 结论:细胞内TG或Ch含量对VLDL受体的调节作用微弱,与TG相比,Ch的调节作用更弱。

The regulation of the VLDL receptor on mouse peritoneal macrophages was studied.By preincubation of cells with TC-enriched VLDL, the maximum binding capacity (Bmax)of cells for 125I-VLDL (1071 ng/mg cell protein) was decreased by 5% only as compared with control cells (1127 ng/mg), 2.5-fold increase of intrace-llular TG contents resulted in decrease of uptake and degradation of 125I-VLDL abont 40% and 22% respectively.By preincubation of cells with Ac-LDL, the Bmax for 125I-VLDL (633ng/mg) was decreased by 14% only as compared with control cells (831 ng/mg);the uptake and degradation were decreased by 10% and 21%,respectively, although the cellular Ch was increased 23-fold.Then, with more increase of cellular TG or Ch, the uptake and degradation of 125I-VLDL were unchanged.From these results, we concluded that VLDL receptor is only slightly down-regulated by TG or Ch loading, compared with TG, Ch was less effective in regulation.