Sphingosylphosphorylcholines (SPC)
Sphingosylphosphorylcholine (SPC) has been identified in normal blood plasma, ascites and various other tissues. SPC is similar in structure to sphingosine-1-phosphate and lyso-phosphatidylcholine and has at least low-binding affinity to some of the same receptors such as the sphingosine-1-phosphate receptor. SPC is a bioactive lipid that acts as an intracellular and extracellular signaling molecule in numerous biological processes and activates various signaling cascades. It acts by binding to and activating cell surface receptors and thereby triggers numerous cellular responses. Some of these signaling responses include vasoconstriction, vasodilation, angiogenesis, stress fiber formation, cytoskeletal rearrangements, proliferation, differentiation, migration, wound healing, and stimulation of DNA synthesis. SPC can also inhibit the growth of various cell types, mostly those of tumor cells, causing much interest in its possible role as an anti-tumor therapy. SPC is a high-affinity ligand for the orphan receptor ovarian cancer G-protein-coupled receptor 1 (OGR1). The specific binding of SPC to OGR1 also activates p42/44 mitogen-activated protein kinases (MAP kinases) and inhibits cell proliferation.1 D-erythro-SPC, but not L-threo-SPC, stereoselectively stimulates the proliferation of human adipose tissue-derived mesenchymal stem cells.2 SPC has also been shown to cause an increase in urine production in the kidneys with an abnormal accumulation of salt.3
References:
- Y. Xu et al. “Sphingosylphosphorylcholine is a ligand for ovarian cancer G-protein-coupled receptor 1” Nature Cell Biology, Vol. 2:5 pp. 261-267, 2000
- J. Kim et al. “Sphingosylphosphorylcholine induces proliferation of human adipose tissue-derived mesenchymal stem cells via activation of JNK” Journal of Lipid Research, Vol. 47 pp. 653-664, 2006
- A. Huwiler et al. “Sphingosylphosphorylcholine acts in an anti-inflammatory manner in renal mesangial cells by reducing interleukin-1ß-induced prostaglandin E2 formation” Journal of Lipid Research, Vol. 48 pp. 1985, 2007