Hendriks W L, Van Vark L C, Schoonderwoerd K, Jansen H, Havekes L M
TNO Prevention and Health, Gaubius Laboratory, Zernikedreef 9, 2333 CK Leiden, P.O. Box 2215, 2301 CE Leiden, The Netherlands.
Biochem J. 1998 Mar 1;330 ( Pt 2)(Pt 2):765-9. doi: 10.1042/bj3300765.
Lipoprotein lipase (LPL) purified from bovine milk showed variable abilities to stimulate the binding of low density lipoprotein (LDL) to J774 macrophages. The presence of a 37 kDa protein in the LPL sample seemed to be of importance for its stimulatory capacity. In order to investigate this, we isolated LPL from bovine milk via heparin Sepharose chromatography using a continuous salt gradient. Fractions containing the 37 kDa protein (as shown by SDS/PAGE under reducing conditions) eluted first from the column, followed by the 56 kDa LPL protein. The LPL enzymatic activity co-eluted with the 56 kDa protein, whereas the amount of 37 kDa protein fully paralleled the stimulatory effect on the binding of LDL to J774 cells. Samples not containing the 37 kDa protein were far less effective in stimulating the binding. Western blotting using a monoclonal antibody 5D2 against amino acids 396-405 in the carboxy-terminal domain of LPL, showed that the 37 kDa protein may be the C-terminal domain of LPL, presumably generated by proteolytic degradation of the mature LPL protein by milk proteases during its isolation. Furthermore, the functional mass of LPL for stimulation of the binding of LDL, as determined by radiation inactivation, was shown to be 30.9+/-1.8 kDa. We therefore suggest that cleavage of LPL at protease-sensitive sites causes a conformational change, generating an LPL protein which is more effective in mediating the binding and uptake of lipoproteins by cells.
从牛乳中纯化得到的脂蛋白脂肪酶(LPL)刺激低密度脂蛋白(LDL)与J774巨噬细胞结合的能力存在差异。LPL样品中一种37 kDa的蛋白质似乎对其刺激能力至关重要。为了对此进行研究,我们通过使用连续盐梯度的肝素琼脂糖层析从牛乳中分离LPL。含有37 kDa蛋白质的组分(在还原条件下经SDS/PAGE显示)首先从柱中洗脱出来,随后是56 kDa的LPL蛋白质。LPL酶活性与56 kDa蛋白质共洗脱,而37 kDa蛋白质的量与对LDL与J774细胞结合的刺激作用完全平行。不含37 kDa蛋白质的样品在刺激结合方面效果要差得多。使用针对LPL羧基末端结构域中氨基酸396 - 405的单克隆抗体5D2进行的蛋白质印迹分析表明,37 kDa蛋白质可能是LPL的C末端结构域,推测是在其分离过程中由乳蛋白酶对成熟LPL蛋白质进行蛋白水解降解产生的。此外,通过辐射失活测定,刺激LDL结合的LPL功能质量为30.9±1.8 kDa。因此,我们认为LPL在蛋白酶敏感位点的切割会导致构象变化,产生一种在介导细胞对脂蛋白的结合和摄取方面更有效的LPL蛋白质。