Sphingosylphosphorylcholine Stimulates CCL2 Production from Human Umbilical Vein Endothelial Cells

Title
Sphingosylphosphorylcholine Stimulates CCL2 Production from Human Umbilical Vein Endothelial Cells
Author(s)
백석환이화영[이화영]이선영[이선영]김상두[김상두]심재웅[심재웅]김학정[김학정]정영수[정영수]권재영[권재영]정준호[정준호]배외식[배외식]
Keywords
CHEMOATTRACTANT PROTEIN-1 GENE; HIGH-DENSITY-LIPOPROTEIN; NF-KAPPA-B; MONOCYTE ADHESION; APOLIPOPROTEIN-E; ATHEROSCLEROSIS; ACTIVATION; MICE; LYSOSPHINGOLIPIDS; PATHWAYS
Issue Date
201103
Publisher
AMER ASSOC IMMUNOLOGISTS
Citation
JOURNAL OF IMMUNOLOGY, v.186, no.7, pp.4347 - 4353
Abstract
Sphingosylphosphorylcholine (SPC) is a component of high-density lipoprotein particles. We investigated the functional role of SPC in HUVECs. SPC stimulation induced production of the CCL2 chemokine in a PTX-sensitive G-protein-dependent manner. SPC treatment caused the activation of NF-kappa B and AP-1, which are essential for SPC-induced CCL2 production, and induced the activation of three MAPKs, ERK, p38 MAPK, and JNK. Inhibition of p38 MAPK or JNK by specific inhibitors caused a dramatic decrease in SPC-induced CCL2 production. The Jak/STAT3 pathway was also activated upon SPC stimulation of HUVECs. Pretreatment with a Jak inhibitor blocked not only SPC-induced p38 MAPK and JNK activation, but also NF-kappa B and AP-1 activation. Our results suggest that SPC stimulates HUVECs, resulting in Jak/STAT3-, NF-kappa B-, and AP-1-mediated CCL2 production. We also observed that SPC stimulated expression of the adhesion molecule ICAM-1 in HUVECs. Our results suggest that SPC may contribute to atherosclerosis; therefore, SPC and its unidentified target receptor offer a starting point for the development of a treatment for atherosclerosis. The Journal of Immunology, 2011, 186: 4347-4353.
URI
http://hdl.handle.net/YU.REPOSITORY/25549http://dx.doi.org/10.4049/jimmunol.1002068
ISSN
0022-1767
Appears in Collections:
의과대학 > 생화학.분자생물학교실 > Articles
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