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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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  • 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
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    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
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  • 4
    Online Resource
    Online Resource
    Endothelial activation in atherogenesis -selective gene induction of adhesion molecules and growth factors by lysophosphatidylcholine
    Elsevier BV ; 1994
    In:  Pathophysiology Vol. 1 ( 1994-11), p. 334-
    Details
    In: Pathophysiology, Elsevier BV, Vol. 1 ( 1994-11), p. 334-
    Type of Medium: Online Resource
    ISSN: 0928-4680
    URL: Article
    DOI: 10.1016/0928-4680(94)90685-8
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1994
    detail.hit.zdb_id: 2031212-X
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  • 5
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    Online Resource
    Roles of vascular endothelium in atherogenesis.
    Japanese Society of Inflammation and Regeneration ; 1995
    In:  Ensho Vol. 15, No. 5 ( 1995), p. 371-375
    Details
    In: Ensho, Japanese Society of Inflammation and Regeneration, Vol. 15, No. 5 ( 1995), p. 371-375
    Type of Medium: Online Resource
    ISSN: 0389-4290 , 1884-4006
    Uniform Title: 粥状動脈硬化における血管内皮細胞の役割　白血球接着分子および血管平滑筋増殖因子の発現
    URL: Article
    DOI: 10.2492/jsir1981.15.371
    Language: Japanese
    Publisher: Japanese Society of Inflammation and Regeneration
    Publication Date: 1995
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  • 6
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    Online Resource
    Tyrosine Phosphorylation of Platelet Endothelial Cell Adhesion Molecule-1 Induced by Lysophosphatidylcholine in Cultured Endothelial Cells
    Elsevier BV ; 1998
    In:  Biochemical and Biophysical Research Communications Vol. 243, No. 3 ( 1998-02), p. 862-868
    Details
    In: Biochemical and Biophysical Research Communications, Elsevier BV, Vol. 243, No. 3 ( 1998-02), p. 862-868
    Type of Medium: Online Resource
    ISSN: 0006-291X
    URL: Article
    DOI: 10.1006/bbrc.1998.8198
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1998
    detail.hit.zdb_id: 1461396-7
    SSG: 12
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  • 7
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    Lysophosphatidylcholine phosphorylates CREB and activates the jun2TRE site of c‐jun promoter in vascular endothelial cells
    Wiley ; 1999
    In:  FEBS Letters Vol. 457, No. 2 ( 1999-08-27), p. 241-245
    Details
    In: FEBS Letters, Wiley, Vol. 457, No. 2 ( 1999-08-27), p. 241-245
    Abstract: Lysophosphatidylcholine (lyso‐PC), a polar phospholipid increased in atherogenic lipoproteins and atherosclerotic lesions, has been shown to induce transcription of a variety of endothelial genes relevant to atherogenesis. Lyso‐PC has been shown to activate c‐jun N‐terminal kinase (JNK) and activator protein 1 (AP‐1) and thereby stimulate transcription of the c‐jun gene. Here we provide evidence that lyso‐PC can phosphorylate cyclic AMP responsive element binding protein (CREB) and thereby activate the jun2 12‐ O ‐tetradecanoylphorbol 13‐acetate response element (jun2TRE) site of the c‐jun promoter, which appears to be the major molecular mechanism involved in lyso‐PC‐induced c‐jun gene expression in cultured bovine aortic endothelial cells (BAEC). Transient transfection of BAEC with a 1.6‐kbp c‐jun promoter and luciferase reporter fusion gene resulted in a 12.9‐fold increase in luciferase activity by lyso‐PC treatment. Serial deletion mutation in c‐jun promoter and luciferase reporter gene assay revealed that the 5′ promoter region between nucleotide numbers −268 and −127, which contains a jun2TRE binding sequence, was most crucial for lyso‐PC‐induced transcription. The 5′ promoter region between −76 and −27, which contains an AP‐1 site, also affected lyso‐PC‐induced transcription of the c‐jun gene. Point mutation in the jun2TRE site reduced lyso‐PC‐induced transcription of the c‐jun promoter‐luciferase fusion gene by a 70.3% decrease in c‐jun promoter activity. Electrophoretic mobility shift assays showed increased binding of 32 P‐labeled oligonucleotides with jun2TRE in nuclear extracts isolated from lyso‐PC‐treated BAEC, which was abolished or supershifted by anti‐CREB antibody. Immunoblotting with anti‐phosphorylated CREB antibody showed rapid phosphorylation of this protein after lyso‐PC treatment. These results indicate that lyso‐PC phosphorylates CREB, which was then bound to the jun2TRE site of the c‐jun promoter and activated transcription. Activation of jun2TRE may play a key role in the transcriptional activation of c‐jun as well as other endothelial genes depending upon these transcription factors.
    Type of Medium: Online Resource
    ISSN: 0014-5793 , 1873-3468
    URL: Article
    DOI: 10.1016/S0014-5793(99)01049-2
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 1999
    detail.hit.zdb_id: 1460391-3
    SSG: 12
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  • 8
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    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
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