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dc.contributor.author백석환ko
dc.contributor.author이화영[이화영]ko
dc.contributor.author이선영[이선영]ko
dc.contributor.author김상두[김상두]ko
dc.contributor.author심재웅[심재웅]ko
dc.contributor.author김학정[김학정]ko
dc.contributor.author정영수[정영수]ko
dc.contributor.author권재영[권재영]ko
dc.contributor.author정준호[정준호]ko
dc.contributor.author배외식[배외식]ko
dc.date.accessioned2015-12-17T01:32:28Z-
dc.date.available2015-12-17T01:32:28Z-
dc.date.created2015-11-13-
dc.date.issued201103-
dc.identifier.citationJOURNAL OF IMMUNOLOGY, v.186, no.7, pp.4347 - 4353-
dc.identifier.issn0022-1767-
dc.identifier.urihttp://hdl.handle.net/YU.REPOSITORY/25549-
dc.identifier.urihttp://dx.doi.org/10.4049/jimmunol.1002068-
dc.description.abstractSphingosylphosphorylcholine (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.-
dc.language영어-
dc.publisherAMER ASSOC IMMUNOLOGISTS-
dc.subjectCHEMOATTRACTANT PROTEIN-1 GENE-
dc.subjectHIGH-DENSITY-LIPOPROTEIN-
dc.subjectNF-KAPPA-B-
dc.subjectMONOCYTE ADHESION-
dc.subjectAPOLIPOPROTEIN-E-
dc.subjectATHEROSCLEROSIS-
dc.subjectACTIVATION-
dc.subjectMICE-
dc.subjectLYSOSPHINGOLIPIDS-
dc.subjectPATHWAYS-
dc.titleSphingosylphosphorylcholine Stimulates CCL2 Production from Human Umbilical Vein Endothelial Cells-
dc.typeArticle-
dc.identifier.wosid000288751200061-
dc.identifier.scopusid2-s2.0-79955033806-
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의과대학 > 생화학.분자생물학교실 > Articles
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