Lindstedt K A
Wihuri Research Institute, Helsinki, Finland.
J Biol Chem. 1993 Apr 15;268(11):7741-6.
Mast cells and macrophages coexist in the human arterial intima where oxidation of low density lipoproteins (LDL) also takes place during atherosclerosis. To investigate whether mast cells play a role in macrophage-mediated oxidation of LDL, a model system was designed in which mast cells and macrophages were cocultured in incubation medium containing LDL. Stimulation of rat serosal mast cells to induce exocytosis of their cytoplasmic granules was found to inhibit macrophage-mediated oxidation of LDL. The inhibitory effect depended on the ability of mast cell-derived histamine, released from the exocytosed granules into the medium, to bind the copper ions necessary for propagation of the macrophage-initiated oxidation of LDL. In addition to binding free copper ions, the mast cell-derived histamine was also capable of inhibiting oxidation of LDL propagated by copper ions bound to the apolipoprotein B component of the LDL particle. The results indicate that mast cells may prevent cell-mediated oxidation of LDL and imply a potentially preventive role for the mast cell in atherosclerosis.
肥大细胞和巨噬细胞共存于人类动脉内膜中，在动脉粥样硬化过程中低密度脂蛋白（LDL）的氧化也发生在此处。为了研究肥大细胞是否在巨噬细胞介导的LDL氧化中发挥作用，设计了一个模型系统，其中肥大细胞和巨噬细胞在含有LDL的孵育培养基中共培养。结果发现，刺激大鼠浆膜肥大细胞诱导其胞质颗粒胞吐可抑制巨噬细胞介导的LDL氧化。这种抑制作用取决于肥大细胞衍生的组胺从胞吐颗粒释放到培养基中后，与巨噬细胞启动的LDL氧化传播所需的铜离子结合的能力。除了结合游离铜离子外，肥大细胞衍生的组胺还能够抑制由与LDL颗粒载脂蛋白B成分结合的铜离子介导的LDL氧化。结果表明，肥大细胞可能会阻止细胞介导的LDL氧化，并暗示肥大细胞在动脉粥样硬化中可能具有预防作用。
