Dijkstra J, van Galen M, Regts D, Scherphof G
Eur J Biochem. 1985 Apr 15;148(2):391-7. doi: 10.1111/j.1432-1033.1985.tb08851.x.
We investigated the intracellular metabolic fate of [Me-14C]choline-labeled phosphatidylcholines and sphingomyelin taken up by rat Kupffer cells in maintenance culture during interaction with large unilamellar liposomes composed of cholesterol, labeled choline-phospholipid and phosphatidylserine (molar ration 5:4:1). With both labeled compounds only small proportions of water-soluble radioactivity were found to accumulate in the cells and in the culture medium, suggesting limited phospholipid degradation. However, after a lag period of 30 min progressively increasing proportions of cell-associated liposomal phospholipid were found to be converted to cellular phospholipid, nearly all of which was phosphatidylcholine. This conversion as well as the limited release of water-soluble label from the cells was inhibited by the lysosomotropic agents ammonium chloride and chloroquine. With [Me-14C]choline-labeled lysophosphatidylcholine, label was found to become cell-associated far in excess of an encapsulated liposomal label, [3H]inulin. Without a lag period virtually all of this was rapidly converted to phosphatidylcholine, a process which was not inhibited by the lysosomotropic agents. It is concluded that Kupffer cells, after endocytosis of liposomes, degrade the liposomal phospholipids effectively but reutilize the choline moiety for de novo synthesis of cellular phosphatidylcholine.
我们研究了在维持培养中，与由胆固醇、标记的胆碱磷脂和磷脂酰丝氨酸（摩尔比5:4:1）组成的大单层脂质体相互作用时，大鼠库普弗细胞摄取的[甲基-14C]胆碱标记的磷脂酰胆碱和鞘磷脂的细胞内代谢命运。对于这两种标记化合物，仅发现少量水溶性放射性在细胞和培养基中积累，表明磷脂降解有限。然而，在30分钟的延迟期后，发现细胞相关脂质体磷脂转化为细胞磷脂的比例逐渐增加，其中几乎全部是磷脂酰胆碱。氯化铵和氯喹这两种溶酶体促渗剂抑制了这种转化以及细胞中水溶性标记物的有限释放。对于[甲基-14C]胆碱标记的溶血磷脂酰胆碱，发现标记物与细胞结合的量远远超过包裹的脂质体标记物[3H]菊粉。几乎所有的溶血磷脂酰胆碱在没有延迟期的情况下迅速转化为磷脂酰胆碱，这一过程不受溶酶体促渗剂的抑制。得出的结论是，库普弗细胞在摄取脂质体后，有效地降解脂质体磷脂，但重新利用胆碱部分用于细胞磷脂酰胆碱的从头合成。
