Prokazova N V, Zvezdina N D, Korotaeva A A
Institute of Experimental Cardiology, Cardiology Research Center, Moscow, Russia.
Biochemistry (Mosc). 1998 Jan;63(1):31-7.
Lysophosphatidylcholine (LPC), 1-acyl-sn-glycero-3-phosphocholine, is well known as an intermediate of metabolism of phosphatidylcholine (PC), the main phospholipid component in all eukaryotic and many prokaryotic cells. LPC is produced as a result of PC hydrolysis by several isoforms of phospholipase A2 (PLA2) and in the reaction mediated by lecithin-cholesterol acyltransferase that transfers the fatty acid residue from PC to cholesterol. LPC is classified as a second messengers that is produced by activation of cytosolic hormone-activated PLA2. It was shown that LPC inhibits transmembrane signaling via receptors, which in their active form are linked to G-proteins. There is a viewpoint that LPC abolishes formation of the complex between the receptor and G-protein. The effect of LPC on protein kinase C (PKC) activation is considered in this review. It was shown that low (less than 20 microM) and high (more than 30 microM) concentrations of LPC activated and inhibited PKC, respectively. The mechanism of LPC-induced activation of PKC still remains unclear. However, the studies of the effect of LPC on signal transduction through the PKC-mediated pathway showed that LPC probably plays an auxiliary role. It was suggested that LPC may prolong the effect of the direct activators of PKC (such as 1,2-diacylglycerol or phorbol esters). The physiological role of the elevation of LPC level in tissues is associated with its ability to enhance or even evoke cell proliferation, stimulate adhesion and differentiation of lymphoid cells, have mitogenic effect on macrophages, activate human T-lymphocytes, initiate monocyte chemotaxis, decrease myocardial sensitivity to cholinergic stimulation, impair contractility of arterial smooth muscle, and modulate aggregation of platelets.
溶血磷脂酰胆碱（LPC），即1-酰基-sn-甘油-3-磷酸胆碱，是磷脂酰胆碱（PC）代谢的中间产物，PC是所有真核细胞和许多原核细胞中的主要磷脂成分。LPC是由磷脂酶A2（PLA2）的几种同工型水解PC产生的，也是在卵磷脂胆固醇酰基转移酶介导的反应中产生的，该酶将脂肪酸残基从PC转移到胆固醇上。LPC被归类为一种第二信使，由胞质激素激活的PLA2激活产生。研究表明，LPC通过受体抑制跨膜信号传导，这些受体的活性形式与G蛋白相连。有一种观点认为，LPC会消除受体与G蛋白之间复合物的形成。本综述考虑了LPC对蛋白激酶C（PKC）激活的影响。研究表明，低浓度（低于20微摩尔）和高浓度（高于30微摩尔）的LPC分别激活和抑制PKC。LPC诱导PKC激活的机制仍不清楚。然而，对LPC通过PKC介导的途径对信号转导影响的研究表明，LPC可能起辅助作用。有人认为，LPC可能会延长PKC直接激活剂（如1,2-二酰基甘油或佛波酯）的作用。组织中LPC水平升高的生理作用与其增强甚至诱发细胞增殖、刺激淋巴细胞黏附和分化、对巨噬细胞有促有丝分裂作用、激活人T淋巴细胞、引发单核细胞趋化性、降低心肌对胆碱能刺激的敏感性、损害动脉平滑肌收缩力以及调节血小板聚集的能力有关。
