• J Redox biol (2022): 102556.

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.

Reference:
[1]. Matsumoto, T., Kobayashi, T., and Kamata, K. Role of lysophosphatidylcholine (LPC) in atherosclerosis. Curr. Med. Chem. 14(30), 3209-3220 (2007).
[2]. Lauber, K., Bohn, E., Krober, S.M., et al. Apoptotic cells induce migration of phagocytes via caspase-3-mediated release of a lipid attraction signal. Cell. 113(6), 717-730 (2003).
[3]. Woodruff, R.H., and Franklin, R.J. Demyelination and remyelination of the caudal cerebellar peduncle of adult rats following stereotaxic injections of lysolecithin, ethidium bromide, and complement/anti-galactocerebroside: A comparative study. Glia. 25(3), 216-228 (1999).