Gelissen I C, Hochgrebe T, Wilson M R, Easterbrook-Smith S B, Jessup W, Dean R T, Brown A J
Cell Biology Unit, Heart Research Institute, 145-147 Missenden Road, Camperdown, Sydney, N.S.W. 2050, Australia.
Biochem J. 1998 Apr 1;331 ( Pt 1)(Pt 1):231-7. doi: 10.1042/bj3310231.
Apolipoprotein J (apo J) is a secreted glycoprotein of which the exact function remains a matter for speculation. Apo J has been implicated in such diverse processes as sperm maturation, regulation of complement activation, programmed cell death, tissue remodelling and lipid transport. In this study a possible role for apo J in lipid transport was explored. Mouse peritoneal macrophages were incubated with acetylated low-density lipoprotein (AcLDL) to produce foam cells containing cholesterol and cholesteryl esters. Incubation of the foam cells with physiological concentrations of purified apo J led to a dose-dependent export of cholesterol. The appearance of cholesterol in the medium was associated predominantly with a decline in intracellular cholesteryl esters rather than intracellular free cholesterol. The kinetics of cholesterol release to apo J were similar to apo A-I, an established promoter of cholesterol efflux. Apo J was also shown to induce phospholipid efflux from cells, whereas the cholesterol exported to the medium was associated with the apo J. Studies using foam cells from apo E-null mice showed that the cholesterol exported to the medium was independent of apo E production by the cells. These results present the first evidence that apo J can promote cholesterol efflux from foam cells and indicates that it might have a function in cellular cholesterol homoeostasis in both normal and pathological situations.
载脂蛋白J（apo J）是一种分泌型糖蛋白，其确切功能仍有待推测。Apo J参与了多种不同的过程，如精子成熟、补体激活调节、程序性细胞死亡、组织重塑和脂质运输。在本研究中，探讨了apo J在脂质运输中的可能作用。将小鼠腹腔巨噬细胞与乙酰化低密度脂蛋白（AcLDL）孵育，以产生含有胆固醇和胆固醇酯的泡沫细胞。用生理浓度的纯化apo J孵育泡沫细胞导致胆固醇呈剂量依赖性输出。培养基中胆固醇的出现主要与细胞内胆固醇酯的减少有关，而不是细胞内游离胆固醇的减少。胆固醇向apo J释放的动力学与apo A-I相似，apo A-I是一种已确定的胆固醇流出促进剂。Apo J还被证明可诱导细胞内磷脂流出，而输出到培养基中的胆固醇与apo J相关。使用载脂蛋白E基因敲除小鼠的泡沫细胞进行的研究表明，输出到培养基中的胆固醇与细胞产生的载脂蛋白E无关。这些结果首次证明apo J可以促进泡沫细胞中的胆固醇流出，并表明它可能在正常和病理情况下的细胞胆固醇稳态中发挥作用。
