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We are analyzing https://link.springer.com/article/10.1007/s00395-005-0582-z.

Title:
The antiatherogenic and antiinflammatory effect of HDL–associated lysosphingolipids operates via Akt ➞NF–kappaB signalling pathways in human vascular endothelial cells | Basic Research in Cardiology
Description:
Adhesion of mononuclear cells to the vascular endothelium and their subsequent transmigration into the arterial wall represent key events in the pathogenesis of arteriosclerosis. In previous studies we have shown that high density lipoproteins (HDL) and the HDL–associated sphingosylphosphorylcholine (SPC) have the ability to suppress the TNF–alpha–induced expression of endothelial cell E–selectin. However, the current understanding of the mechanism by which HDL reduces the expression of E–selectin is still incomplete. In the present study we show that interaction of the HDL–associated sphingosylphosphorylcholine and sphingosylgalactosyl–3–sulfate (lysosulfatide, LSF) with the G–protein–coupled EDG receptor initiates a signalling cascade that activates the protein kinase Akt and reduces the E–selectin, ICAM–1 and VCAM–1 expression on protein and mRNA level. This signalling cascade is consistently associated with a reduced translocation of TNF–alpha–activated NF–kappaB into the cell nucleus. The suppressor effect of SPC and LSF is completely reverted by inhibition of the phosphatidylinositol– 3–kinase/Akt pathway. We conclude that the antiatherogenic/antiinflammatory effect of lysosphingolipids depends on a competitive interaction of EDG receptor–induced inhibition and TNF–alpha–initiated stimulation of NF–kappaB translocation into the cell nucleus thereby preventing or stimulating inflammatory events in atherogenesis.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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  • Education
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Custom-built

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {🔍}

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Topics {✒️}

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Schema {🗺️}

WebPage:
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         headline:The antiatherogenic and antiinflammatory effect of HDL–associated lysosphingolipids operates via Akt ➞NF–kappaB signalling pathways in human vascular endothelial cells
         description:Adhesion of mononuclear cells to the vascular endothelium and their subsequent transmigration into the arterial wall represent key events in the pathogenesis of arteriosclerosis. In previous studies we have shown that high density lipoproteins (HDL) and the HDL–associated sphingosylphosphorylcholine (SPC) have the ability to suppress the TNF–alpha–induced expression of endothelial cell E–selectin. However, the current understanding of the mechanism by which HDL reduces the expression of E–selectin is still incomplete. In the present study we show that interaction of the HDL–associated sphingosylphosphorylcholine and sphingosylgalactosyl–3–sulfate (lysosulfatide, LSF) with the G–protein–coupled EDG receptor initiates a signalling cascade that activates the protein kinase Akt and reduces the E–selectin, ICAM–1 and VCAM–1 expression on protein and mRNA level. This signalling cascade is consistently associated with a reduced translocation of TNF–alpha–activated NF–kappaB into the cell nucleus. The suppressor effect of SPC and LSF is completely reverted by inhibition of the phosphatidylinositol– 3–kinase/Akt pathway. We conclude that the antiatherogenic/antiinflammatory effect of lysosphingolipids depends on a competitive interaction of EDG receptor–induced inhibition and TNF–alpha–initiated stimulation of NF–kappaB translocation into the cell nucleus thereby preventing or stimulating inflammatory events in atherogenesis.
         datePublished:2006-02-06T00:00:00Z
         dateModified:2006-02-06T00:00:00Z
         pageStart:109
         pageEnd:116
         sameAs:https://doi.org/10.1007/s00395-005-0582-z
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            Cardiology
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            name:Basic Research in Cardiology
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               0300-8428
            volumeNumber:101
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               name:A. Schmidt
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                     name:Molecular–Cardiology University of Münster
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      headline:The antiatherogenic and antiinflammatory effect of HDL–associated lysosphingolipids operates via Akt ➞NF–kappaB signalling pathways in human vascular endothelial cells
      description:Adhesion of mononuclear cells to the vascular endothelium and their subsequent transmigration into the arterial wall represent key events in the pathogenesis of arteriosclerosis. In previous studies we have shown that high density lipoproteins (HDL) and the HDL–associated sphingosylphosphorylcholine (SPC) have the ability to suppress the TNF–alpha–induced expression of endothelial cell E–selectin. However, the current understanding of the mechanism by which HDL reduces the expression of E–selectin is still incomplete. In the present study we show that interaction of the HDL–associated sphingosylphosphorylcholine and sphingosylgalactosyl–3–sulfate (lysosulfatide, LSF) with the G–protein–coupled EDG receptor initiates a signalling cascade that activates the protein kinase Akt and reduces the E–selectin, ICAM–1 and VCAM–1 expression on protein and mRNA level. This signalling cascade is consistently associated with a reduced translocation of TNF–alpha–activated NF–kappaB into the cell nucleus. The suppressor effect of SPC and LSF is completely reverted by inhibition of the phosphatidylinositol– 3–kinase/Akt pathway. We conclude that the antiatherogenic/antiinflammatory effect of lysosphingolipids depends on a competitive interaction of EDG receptor–induced inhibition and TNF–alpha–initiated stimulation of NF–kappaB translocation into the cell nucleus thereby preventing or stimulating inflammatory events in atherogenesis.
      datePublished:2006-02-06T00:00:00Z
      dateModified:2006-02-06T00:00:00Z
      pageStart:109
      pageEnd:116
      sameAs:https://doi.org/10.1007/s00395-005-0582-z
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         HDL
         lysosphingolipids
         cell adhesion molecules
         NF–kappaB
         endothelial cells
         Cardiology
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      isPartOf:
         name:Basic Research in Cardiology
         issn:
            1435-1803
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         volumeNumber:101
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            Periodical
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            name:A. Schmidt
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                  name:Molecular–Cardiology University of Münster
                  address:
                     name:Leibniz–Institute of Arteriosclerosis Research, Molecular–Cardiology University of Münster, Münster, Germany
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                  type:Organization
            email:[email protected]
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            name:S. Geigenmüller
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                  name:Molecular–Cardiology University of Münster
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                     name:Leibniz–Institute of Arteriosclerosis Research, Molecular–Cardiology University of Münster, Münster, Germany
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                     name:Leibniz–Institute of Arteriosclerosis Research, Molecular–Cardiology University of Münster, Münster, Germany
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            name:E. Buddecke
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                  name:Molecular–Cardiology University of Münster
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                     name:Leibniz–Institute of Arteriosclerosis Research, Molecular–Cardiology University of Münster, Münster, Germany
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         name:Leibniz–Institute of Arteriosclerosis Research, Molecular–Cardiology University of Münster, Münster, Germany
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               name:Leibniz–Institute of Arteriosclerosis Research, Molecular–Cardiology University of Münster, Münster, Germany
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      name:S. Geigenmüller
      affiliation:
            name:Molecular–Cardiology University of Münster
            address:
               name:Leibniz–Institute of Arteriosclerosis Research, Molecular–Cardiology University of Münster, Münster, Germany
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            name:Molecular–Cardiology University of Münster
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               name:Leibniz–Institute of Arteriosclerosis Research, Molecular–Cardiology University of Münster, Münster, Germany
               type:PostalAddress
            type:Organization
      name:E. Buddecke
      affiliation:
            name:Molecular–Cardiology University of Münster
            address:
               name:Leibniz–Institute of Arteriosclerosis Research, Molecular–Cardiology University of Münster, Münster, Germany
               type:PostalAddress
            type:Organization
            name:University of Münster
            address:
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      name:Leibniz–Institute of Arteriosclerosis Research, Molecular–Cardiology University of Münster, Münster, Germany
      name:Leibniz–Institute of Arteriosclerosis Research, Molecular–Cardiology University of Münster, Münster, Germany
      name:Institute of Physiological Chemistry and Pathobiochemistry, University of Münster, Münster, Germany
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