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  • Online Resource  (4)
  • Ovid Technologies (Wolters Kluwer Health)  (4)
  • Nishi, Eiichiro  (4)
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  • Online Resource  (4)
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  • Ovid Technologies (Wolters Kluwer Health)  (4)
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  • 1
    Online Resource
    Online Resource
    Ligand Specificity of LOX-1, a Novel Endothelial Receptor for Oxidized Low Density Lipoprotein
    Ovid Technologies (Wolters Kluwer Health) ; 1998
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 18, No. 10 ( 1998-10), p. 1541-1547
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 18, No. 10 ( 1998-10), p. 1541-1547
    Abstract: Abstract —Endothelial dysfunction, or activation, elicited by oxidized low density lipoprotein (Ox-LDL) and its lipid constituents has been shown to play a key role in the pathogenesis of atherosclerosis. We recently have identified a novel receptor for Ox-LDL-designated lectin-like Ox-LDL receptor (LOX-1) in vascular endothelial cells. To examine ligand specificity of LOX-1, we established CHO cell lines stably expressing both human and bovine LOX-1 (LOX-1-CHO). LOX-1-CHO bound and degraded 125 I-labeled Ox-LDL but did not significantly degrade 125 I-labeled acetylated LDL (Ac-LDL). Fucoidin and maleylated BSA (M-BSA), which inhibit 125 I-Ox-LDL binding to class A scavenger receptors, did not inhibit 125 I-Ox-LDL binding or degradation in LOX-1-CHO. Polyinosinic acid and carrageenan, in contrast, significantly reduced 125 I-Ox-LDL binding to LOX-1-CHO by 62% and 60%, respectively. Delipidated and untreated 125 I-Ox-LDL were bound and degraded equally in LOX-1-CHO; furthermore, excess amounts of unlabeled, delipidated Ox-LDL inhibited binding and degradation of untreated 125 I-Ox-LDL. Taken together, LOX-1 is a receptor for Ox-LDL but not for Ac-LDL. LOX-1 recognizes protein moiety of Ox-LDL, and its ligand specificity is distinct from other receptors for Ox-LDL, including class A and B scavenger receptors.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/01.ATV.18.10.1541
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1998
    detail.hit.zdb_id: 1494427-3
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    Online Resource
  • 2
    Online Resource
    Online Resource
    Elevated Levels of cAMP Inhibit Protein Kinase C– Independent Mechanisms of Endothelial Platelet-Derived Growth Factor–B Chain and Intercellular Adhesion Molecule-1 Gene Induction by Lysophosphatidylcholine
    Ovid Technologies (Wolters Kluwer Health) ; 1995
    In:  Circulation Research Vol. 77, No. 3 ( 1995-09), p. 530-535
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 77, No. 3 ( 1995-09), p. 530-535
    Abstract: Abstract Lysophosphatidylcholine (lyso-PC), a polar phospholipid product increased in atherogenic lipoproteins and atherosclerotic lesions, has been shown to differentially induce functional intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 and mRNA for platelet-derived growth factor (PDGF)–A and –B chains and heparin-binding epidermal growth factor–like growth factor in various cultured endothelial cells. In this study, we have demonstrated increased expression of cell- and matrix-associated forms of PDGF–B chain (PDGF-B) protein elicited by lyso-PC and further characterized potential signal transduction mechanisms responsible for lyso-PC–induced gene expression, focusing on PDGF-B and ICAM-1 genes in cultured human umbilical vein endothelial cell models. Cycloheximide almost completely inhibited PDGF-B but not ICAM-1 mRNA induction elicited by lyso-PC, suggesting that dependence on de novo protein synthesis for PDGF-B is different from that for ICAM-1. Prolonged exposure to phorbol myristate acetate (PMA), which depletes protein kinase C (PKC), or staurosporine, a PKC inhibitor, did not block lyso-PC–induced increases in PDGF-B or ICAM-1 mRNA. Forskolin and dibutyryl cAMP, which elevate intracellular cAMP levels, blocked both PDGF-B and ICAM-1 upregulation elicited by lyso-PC; however, these cAMP-elevating agents did not suppress ICAM-1 upregulation by PMA. Taken together, PDGF-B and ICAM-1 gene induction by lyso-PC may involve different signaling mechanisms; however, both appear to be independent of PMA-regulatable PKC activation but are suppressed by increased levels of intracellular cAMP.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.77.3.530
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1995
    detail.hit.zdb_id: 1467838-X
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  • 3
    Online Resource
    Online Resource
    Lysophosphatidylcholine Enhances Cytokine-Induced Interferon Gamma Expression in Human T Lymphocytes
    Ovid Technologies (Wolters Kluwer Health) ; 1998
    In:  Circulation Research Vol. 83, No. 5 ( 1998-09-07), p. 508-515
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 83, No. 5 ( 1998-09-07), p. 508-515
    Abstract: Abstract —Accumulation of substantial numbers of activated T lymphocytes, as well as monocyte/macrophages, in focal areas of arterial intima appears to be a hallmark of atherogenesis. Our previous report demonstrated that lysophosphatidylcholine (lyso-PC), a polar phospholipid component that is increased in atherogenic lipoproteins and atherosclerotic lesions, can upregulate the expression of heparin-binding epidermal growth factor–like growth factor and the interleukin (IL)-2 receptor in cultured human peripheral T lymphocytes. In this study, we show that lyso-PC can also enhance interferon gamma (IFN-γ) secretion and gene expression in human T lymphocytes. Lyso-PC–induced upregulation of IFN-γ depended on the presence of IL-2, IL-12, or phytohemagglutinin in culture media and was similarly observed in both CD4 + and CD8 + subsets. Actinomycin D chase by Northern blotting showed that lyso-PC significantly prolonged IFN-γ mRNA half-lives in human T cells. Transient transfection of IFN-γ promoter-reporter gene construct in the human T-cell line Jurkat cells demonstrated that lyso-PC stimulated the transcription of IFN-γ promoter-driven luciferase gene. Analyses of serial deletion mutations of IFN-γ promoter revealed that the lyso-PC–responsive element is located between base pairs −102 and −78 of the transcription initiation site of the IFN-γ gene. Enhanced expression of IFN-γ in T lymphocytes by lyso-PC may play a crucial role in atherogenesis.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.83.5.508
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1998
    detail.hit.zdb_id: 1467838-X
    Location Call Number Limitation Availability
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    Online Resource
  • 4
    Online Resource
    Online Resource
    Lysophosphatidylcholine Increases Expression of Heparin-Binding Epidermal Growth Factor–Like Growth Factor in Human T Lymphocytes
    Ovid Technologies (Wolters Kluwer Health) ; 1997
    In:  Circulation Research Vol. 80, No. 5 ( 1997-05), p. 638-644
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 80, No. 5 ( 1997-05), p. 638-644
    Abstract: Abstract Atherosclerotic lesions contain substantial numbers of activated T lymphocytes in addition to monocytes/macrophages. T cell–derived cytokines and growth factors may play a role in atherogenesis; however, stimuli responsible for T-cell activation in atherogenesis have not been fully elucidated. In this study, we provide evidence that lysophosphatidylcholine (lyso-PC), a polar phospholipid component increased in atherogenic lipoproteins and atherosclerotic lesions, can upregulate gene expression and secretion of heparin-binding epidermal growth factor–like growth factor (HB-EGF) in cultured T lymphocytes isolated from human peripheral blood. Effects of lyso-PC on T lymphocytes appear to be selective and specific, since lyso-PC also increases interleukin (IL)-2 receptor expression but does not affect mRNA levels for IL-2 or IL-4. Lyso-PC–induced upregulation of HB-EGF and IL-2 receptor mRNA in peripheral T cells is mostly dependent on exogenous IL-2 in conditioned medium. The effect of lyso-PC on HB-EGF induction was more potent in CD4 + cells than in CD8 + cells, although lyso-PC increases IL-2 receptor expression dramatically in both CD4 + cells and CD8 + cells. Lyso-PC similarly increased HB-EGF expression in Jurkat cells, a cell line for human CD4 + T lymphocytes. These results in vitro suggest that lyso-PC may be an important stimulus for T cells in atherogenesis in vivo to upregulate HB-EGF and that T cell–derived smooth muscle growth factors may modulate atherosclerotic progression.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.80.5.638
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1997
    detail.hit.zdb_id: 1467838-X
    Location Call Number Limitation Availability
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