Lysophosphatidylcholines (LPC, lysoPC), also called lysolecithins, are a class of chemical compounds which are derived from phosphatidylcholines.
They result from partial hydrolysis of phosphatidylcholines, which removes one of the fatty acid groups. The hydrolysis is generally the result of the enzymatic action of phospholipase A2. Among other properties, they activate endothelial cells during early atherosclerosis and stimulate phagocyte recruitment when released by apoptotic cells. Moreover, LPCs can be used in the lab to cause demyelination of brain slices, to mimic the effects of demyelinating diseases such as multiple sclerosis. Further, they are known to stimulate phagocytosis of the myelin sheath and can change the surface properties of erythrocytes. LPC-induced demyelination is thought to occur through the actions of recruited macrophages and microglia which phagocytose nearby myelin. Invading T cells are also thought to mediate this process. Bacteria such as Legionella pneumophila utilize phospholipase A2 end-products ( fatty acids and lysophospholipids) to cause host cell (macrophage) apoptosis through cytochrome C release.
LPCs are present as minor phospholipids in the cell membrane (≤ 3%) and in the blood plasma (8-12%). Since LPCs are quickly metabolized by lysophospholipase and LPC-acyltransferase, they last only shortly in vivo. By replacing the acyl-group within the LPC with an alkyl-group, alkyl-lysophospholipids (ALP) were synthesized. These LPC analogues are metabolically stable, and several such as edelfosine, miltefosine and perifosine are under research and development as drugs against cancer and other diseases. Lysophosphatidylcholine processing has been discovered to be an essential component of normal human brain development: those born with genes that prevent adequate uptake suffer from lethal microcephaly.