REVIEW: Effect of Lysophosphatidylcholine on Transmembrane Signal Transduction

N. V. Prokazova^1*, N. D. Zvezdina², and A. A. Korotaeva¹

¹Institute of Experimental Cardiology, Cardiology Research Center, ul. 3-ya Cherepkovskaya 15a, Moscow, 121552 Russia; fax: (095) 415-2962

²Kol'tsov Institute of Developmental Biology, Russian Academy of Sciences, ul. Vavilova 26, Moscow, 117334 Russia; fax: (095) 135-8012

^* To whom correspondence should be addressed.

Received July 14, 1997

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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 µM) and high (more than 30 µM) 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.

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KEY WORDS: lysophosphatidylcholine, phospholipase A₂, G-proteins, protein kinase C

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