Sphingosylphosphorylcholine Stimulates CCL2 Production from Human Umbilical Vein Endothelial Cells

  • Ha Young Lee
    *Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110-799, Korea;
  • Sun Young Lee
    †Department of Biological Sciences, Sungkyunkwan University, Suwon 440-746, Korea;
  • Sang Doo Kim
    †Department of Biological Sciences, Sungkyunkwan University, Suwon 440-746, Korea;
  • Jae Woong Shim
    †Department of Biological Sciences, Sungkyunkwan University, Suwon 440-746, Korea;
  • Hak Jung Kim
    †Department of Biological Sciences, Sungkyunkwan University, Suwon 440-746, Korea;
  • Young Su Jung
    †Department of Biological Sciences, Sungkyunkwan University, Suwon 440-746, Korea;
  • Jae Young Kwon
    †Department of Biological Sciences, Sungkyunkwan University, Suwon 440-746, Korea;
  • Suk-Hwan Baek
    §Department of Biochemistry and Molecular Biology, College of Medicine, Yeungnam University, Daegu 705-030, Korea
  • Junho Chung
    *Cancer Research Institute, College of Medicine, Seoul National University, Seoul 110-799, Korea;
  • Yoe-Sik Bae
    †Department of Biological Sciences, Sungkyunkwan University, Suwon 440-746, Korea;

説明

<jats:title>Abstract</jats:title> <jats:p>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-κB 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-κB and AP-1 activation. Our results suggest that SPC stimulates HUVECs, resulting in Jak/STAT3–, NF-κB–, 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.</jats:p>

収録刊行物

  • The Journal of Immunology

    The Journal of Immunology 186 (7), 4347-4353, 2011-04-01

    The American Association of Immunologists

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