Authors: LEE, Ha-young; SHIN, Eun-ha; BAE, Yoe-sik

Source: Acta Pharmacologica Sinica, Volume 27, Number 10, October 2006 , pp. 1359-1366(8)

Publisher: Wiley-Blackwell

Abstract:

Aim: To investigate the effects of sphingosylphosphorylcholine (SPC) on human monocyte-derived dendritic cell (DC) chemotaxis. Methods: Human DC were generated from peripheral blood monocytes by culturing them with granulocyte macrophage-colony stimulating factor and interleukin-4. The effect of SPC on the DC chemotactic migration was measured by chemotaxis assay. Intracellular signaling event involved in the SPC-induced DC chemotaxis was investigated with several inhibitors for specific kinase. The expression of the SPC receptors was examined by reverse transcription polymerase chain reaction. Results: We found that SPC induced chemotactic migration in immature DC (iDC) and mature DC (mDC). In terms of SPC-induced signaling events, mitogen activated protein kinase activation and Akt activation in iDC and mDC were stimulated. SPC-induced chemotaxis was mediated by extracellular signal-regulated protein kinase and phosphoino-sitide-3-kinase, but not by calcium in both iDC and mDC. Although mDC express ovarian cancer G protein-coupled receptor 1, but not G protein-coupled receptor 4, iDC do not express any of these receptors. To examine the involvement of sphin-gosine-1-phosphate (S1P) receptors, we checked the effect of an S1P receptor antagonist (VPC23019) on SPC-induced DC chemotaxis. VPC23019 did not affect SPC-induced DC chemotaxis. Conclusion: The results suggest that SPC may play a role in regulating DC trafficking during phagocytosis and the T cell-stimulating phase, and the unique SPC receptor, which is different from S 1P receptors, is involved in SPC-induced chemotaxis.

Keywords: dendritic cells; sphingosylphosphorylcho line; chemotaxis; pertussis toxin-sensitive G protein; extracellular signal regulated protein kinase

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1745-7254.2006.00426.x

Publication date: 2006-10-01

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