Fourcade O, Le Balle F, Fauvel J, Simon M F, Chap H
Institut Fédératif de Recherche en Immunologie Cellulaire et Moléculaire, Université Paul Sabatier and Centre Hospitalo-Universitaire de Toulouse, INSERM Unité 326, Toulouse, France.
Adv Enzyme Regul. 1998;38:99-107. doi: 10.1016/s0065-2571(97)00002-2.
Secretory non-pancreatic phospholipase A2 (sPLA2), also called type II-PLA2, is produced in large amounts under inflammatory conditions, thus accumulating in inflammatory fluids. Since the enzyme is virtually inactive on phospholipids from intact cells, we have searched for conditions allowing the action of sPLA2 on membrane phospholipids. Based on an in vitro model, our studies suggest that only those membranes where the transverse distribution of phospholipids has been disturbed offer a convenient surface able to interact with the enzyme, which then achieves significant degradation of all glycerophospholipids. This results in the accumulation of various lysophospholipids such as lysophosphatidylcholine, lysophosphatidylethanolamine and lysophosphatidylserine. However, lysophosphatidic acid (LPA) can also be generated under these conditions involving accumulation of phosphatidic acid in the cytoplasmic leaflet of the membrane, followed by its transfer to the outer monolayer. Since LPA is now considered as a novel phospholipid mediator, this pathway deserves further studies concerning mainly platelets, the main source of LPA identified so far.
分泌型非胰腺磷脂酶A2（sPLA2），也称为II型磷脂酶A2，在炎症条件下大量产生，因此会在炎性液体中积聚。由于该酶对完整细胞的磷脂几乎没有活性，我们一直在寻找能使sPLA2作用于膜磷脂的条件。基于体外模型，我们的研究表明，只有那些磷脂横向分布受到干扰的膜才提供了一个能与该酶相互作用的合适表面，然后该酶能对所有甘油磷脂进行显著降解。这导致了各种溶血磷脂的积累，如溶血磷脂酰胆碱、溶血磷脂酰乙醇胺和溶血磷脂酰丝氨酸。然而，在这些条件下也会产生溶血磷脂酸（LPA），这涉及膜细胞质小叶中磷脂酸的积累，随后转移到外单层。由于LPA现在被认为是一种新型磷脂介质，这条途径值得进一步研究，主要涉及血小板，血小板是迄今为止已确定的LPA的主要来源。
