Lactosylceramides
Lactosylceramide is a very important biochemical as it is not only the precursor of many other glycosphingolipids but many cellular processes are dependent on lactosylceramides. It is the substrate for neutral oligoglycosylceramides, sulfolipids, and gangliosides, all of which possess vital functions. Lactosylceramides also help to stabilize the lipid membrane, activate receptor molecules, and act as a receptor for certain bacteria and toxins. It is expressed on neutrophils and macrophages where it binds to toxins and bacteria during phagocytosis. Its role as a second messenger has been found to be vital for normal processes with deficiencies leading to cancer and inflammation as a result of its neutrophil and anti-inflammatory activities.1 Therefore, lactosylceramide is studied for its use in cancer therapies and as a therapy for other diseases. Other examples of lactosylceramide second messenger functions are tumor necrosis factor alpha and platelet-derived growth factor. A deficiency in the enzyme responsible for hydrolyzing the galactose of lactosylceramide leads to lactosylceramidosis, which is characterized by an accumulation of lactosylceramide resulting in a primary neurological disorder.2 Lactosylceramide is also important in the activation of platelet/endothelial cell adhesion molecule-1 which causes adhesion and diapedesis of monocytes and lymphocytes.3
References:
- Ravinder Pannu et al. “A Novel Role of Lactosylceramide in the Regulation of Tumor Necrosis Factor alpha-mediated Proliferation of Rat Primary Astrocytes: IMPLICATIONS FOR ASTROGLIOSIS FOLLOWING NEUROTRAUMA” Journal of Biological Chemistry, Vol. 280 pp. 13742-13751, 2005
- Glyn Dawson “Glycosphingolipid levels in an unusual neurovisceral storage disease characterized by lactosylceramide galactosyl hydrolase deficiency: lactosylceramidosis” Journal of Lipid Research, Vol. 13 pp. 207-219, 1972
- NanLing Gong “Lactosylceramide recruits PKCα/ε and phospholipase A2 to stimulate PECAM-1 expression in human monocytes and adhesion to endothelial cells” Proceedings of the National Academy of Sciences, Vol. 101:17 pp. 6490-6495, 2004