L-α-Lysophosphatidylcholine from bovine brain 

Contains primarily palmitic, stearic and oleic acids.

Lysophosphatidylcholine is a major component of oxidized low density lipoproteins, and has been implicated in various inflammatory reactions, including atherosclerosis. It is a degradation product of phosphatidylcholine by phospholipase A and has cytolytic properties. The product is used to demyelinate spinal neurons and study the processes underlying remyelination. It activates protein kinase C, p38 MAP kinase, p42 MAP Kinase, and the jun kinase (JNK) pathway, and stimulates transcription of c-jun. Lysophosphatidylcholine accumulates during cardiac ischemia and may induce arrhythmias by uncoupling gap junction communication, and increase ischemic damage by enhancing Na⁺ loading in cardiac myocytes. It also activates TREK1, TREK2 and TRAAK K⁺ channels.

Type V

~99%

−20°C

Lesage, F., et al., Human TREK2, a 2P domain mechano-sensitive K+ channel with multiple regulations by polyunsaturated fatty acids, lysophospholipids and Gs-, Gi- and Gq-protein-coupled receptors. J. Biol. Chem. 275, 28398, (2000)

Huang, Y.H., et al., Lysophosphatidylcholine (LPC) induces proinflammatory cytokines by a platelet-activating factor (PAF) receptor-dependent mechanism. Clin. Exp. Immunol. 116, 326, (1999)

Bassa, B.V., et al., Lysophosphatidylcholine activates mesangial cell PKC and MAP kinase by PLCgamma-1 and tyrosine kinase-Ras pathways. Am. J. Physiol. 277, F328-F337, (1999)

Ousman, S.S. and David, S., Lysophosphatidylcholine induces rapid recruitment and activation of macrophages in the adult mouse spinal cord. Glia 30, 92, (2000)

Daleau, P., Lysophosphatidylcholine, a metabolite which accumulates early in myocardium during ischemia, reduces gap junctional coupling in cardiac cells. J. Mol. Cell. Cardiol. 31, 1391, (1999)

Kita, T., et al., Oxidized-LDL and atherosclerosis. Role of LOX-1. Ann. N.Y. Acad. Sci. 902, 95, (2000)

Chattou, S., et al., Slowly inactivating component of sodium current in ventricular myocytes is decreased by diabetes and partially inhibited by known Na⁺-H⁺ exchange blockers. J. Mol. Cell. Cardiol. 32, 1181, (2000)

Maingret, F., et al., Lysophospholipids open the two-pore domain mechano-gated K⁺ channels TREK-1 and TRAAK. J. Biol. Chem. 275, 10128-10133, (2000)

Ueno, Y., et al., Lysophosphatidylcholine phosphorylates CREB and activates the jun2TRE site of c-jun promoter in vascular endothelial cells. FEBS Lett. 457, 241, (1999)

Jing, Q., et al., Lysophosphatidylcholine activates p38 and p42/44 mitogen-activated protein kinases in monocytic THP-1 cells, but only p38 activation is involved in its stimulated chemotaxis. Circ. Res. 87, 52, (2000)

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