Kokkonen J O, Kovanen P T
Wihuri Research Institute, Helsinki, Finland.
J Lipid Res. 1989 Sep;30(9):1341-8.
Stimulation of rat serosal mast cells in vitro with compound 48/80, a degranulating agent, resulted in an immediate increase in binding of low density lipoproteins (LDL) to the stimulated mast cells. The increase in binding was dose-dependent and closely followed the increase in histamine release, i.e., the exocytosis of mast cell granules. It could be demonstrated that the LDL were bound to exocytosed secretory granules which remained cell-associated. During the recovery period the granule-bound LDL were internalized by the mast cells along with the granules. A single stimulation of mast cells rendered their cytoplasm to be filled with granular material showing positive staining for both apoB and neutral lipid. This change was accompanied by a 30-fold increase in the cellular content of cholesteryl esters. Thus, rat serosal mast cells possess a specific mechanism for uptake of LDL that is activated by stimuli that lead to degranulation, the result being massive uptake of LDL by stimulated mast cells during recovery from degranulation.
用脱颗粒剂化合物48/80体外刺激大鼠浆膜肥大细胞，导致低密度脂蛋白（LDL）与受刺激的肥大细胞的结合立即增加。结合的增加呈剂量依赖性，并紧密跟随组胺释放的增加，即肥大细胞颗粒的胞吐作用。可以证明，LDL与仍与细胞相关的胞吐分泌颗粒结合。在恢复期，颗粒结合的LDL与颗粒一起被肥大细胞内化。对肥大细胞的单次刺激使其细胞质充满颗粒物质，对载脂蛋白B和中性脂质均呈阳性染色。这种变化伴随着胆固醇酯细胞含量增加30倍。因此，大鼠浆膜肥大细胞具有摄取LDL的特定机制，该机制被导致脱颗粒的刺激激活，结果是在从脱颗粒恢复过程中，受刺激的肥大细胞大量摄取LDL。
