Lysophosphatidylcholines are produced by hydrolysis of the fatty acid of phosphatidylcholine at either the sn-1 or sn-2 position by phospholipase A2 (PLA2) or by lecithin-cholesterol acyltranferase (LCAT), which transfers the fatty acid to cholesterol. [1] Lysophosphatidylcholine has effects on a variety of cell types, including smooth muscle cells, endothelial cells, T lymphocytes, monocytes, and macrophages among others. It is a major phospholipid component of oxidized low-density lipoprotein (ox-LDL), and it accumulates in animal models of atherosclerosis. Lysophosphatidylcholine also has pro-inflammatory properties through its activation and modulation of various signaling pathways, including the ERK pathway as well as through protein tyrosine kinase and G protein-coupled receptor (GPCR) signal transduction. It is released from apoptotic cells in vitro following caspase-3 activation of the calcium-independent PLA2 and acts as a chemoattractant for monocytes.[2]  Lysophosphatidylcholine (2 ul, 1%) injected into the caudal cerebellar peduncle of rats induces demyelination of axons in vivo, which are extensively remyelinated by oligodendrocytes six weeks following injection. [3] Lysophosphatidylcholines (egg) is a mixture of lysophosphatidylcholines isolated from chicken egg that has a fatty acid of variable chain length acylated to the sn-1 or sn-2 position.