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We are analyzing https://link.springer.com/article/10.1007/s00394-008-0697-8.

Title:
Conjugated linoleic acid isomers inhibit platelet-derived growth factor-induced NF-κB transactivation and collagen formation in human vascular smooth muscle cells | European Journal of Nutrition
Description:
Background Atherosclerosis is characterized by extensive thickening of the arterial intima partially resulting from deposition of collagen by vascular smooth muscle cells (SMCs). Polyunsaturated fatty acids stimulate collagen formation through NF-κB activation. Aim of the study The present study aimed to explore the effect of conjugated linoleic acids (CLAs) which are known to inhibit NF-κB activation on collagen formation by SMCs. Methods Vascular SMCs were cultured with 50 µmol/l of CLA isomers (c9t11-CLA, t10c12-CLA) or linoleic acid (LA) and analysed for collagen formation and NF-κB p50 transactivation. Results Treatment with CLA isomers but not LA significantly reduced PDGF-stimulated [3H] proline incorporation into cell layer protein of SMCs without altering cell proliferation. Simultaneous treatment with the PPARγ inhibitor T0070907 abrogated this effect. Treatment of SMCs with c9t11-CLA and t10c12-CLA significantly reduced PDGF-induced NF-κB p50 activation. Conclusions CLA isomers inhibit PDGF-stimulated collagen production by vascular SMCs, which is considered to be a hallmark of atherosclerosis, in a PPARγ-dependent manner. Whether inhibition of the NF-κB-pathway is of significance for the reduction of collagen formation by CLA isomers needs further investigation.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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  • Education
  • Science
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Custom-built

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What is the average monthly size of link.springer.com audience?

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


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How Does Link.springer.com Make Money? {💸}

We can't figure out the monetization strategy.

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Keywords {🔍}

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Topics {✒️}

platelet-derived growth factor-bb nf-κb p50 transactivation inhibit nf-κb activation nuclear factor-κb activation month download article/chapter trans-11-conjugated linoleic acid connective tissue macromolecules nf-κb activation collagen formation induced susan gahler & klaus eder erk-mediated il-10 induction nf-kappab independent inhibition conjugated linoleic acid nf-κb-pathway nf-κb pathway conjugated linoleic acids polyunsaturated fatty acids lipopolysaccharide-induced cyclooxygenase human endothelial cells pparγ-dependent mechanism conjugated nonadecadienoic acid pparγ-dependent manner receptor ep1 subtype article european journal full article pdf inhibiting gene expression arachidonic acid metabolism smooth muscle privacy choices/manage cookies cell layer protein α-linolenic acids mesenchymal stem cells nutrition aims attenuate neointima formation subsequent cox-2 expression cysteinyl leukotrien expression linoleic acid collagen genes col1a1 cla isomers pro-inflammatory products nf-kappa european economic area related subjects targeting iκb kinase u937 monocyte adhesion increased 2-methoxyextradiol production vascular cell 5-lipoxygenase activating protein mouse asthma model t10c12-cla

Schema {🗺️}

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         headline:Conjugated linoleic acid isomers inhibit platelet-derived growth factor-induced NF-κB transactivation and collagen formation in human vascular smooth muscle cells
         description:Atherosclerosis is characterized by extensive thickening of the arterial intima partially resulting from deposition of collagen by vascular smooth muscle cells (SMCs). Polyunsaturated fatty acids stimulate collagen formation through NF-κB activation. The present study aimed to explore the effect of conjugated linoleic acids (CLAs) which are known to inhibit NF-κB activation on collagen formation by SMCs. Vascular SMCs were cultured with 50 µmol/l of CLA isomers (c9t11-CLA, t10c12-CLA) or linoleic acid (LA) and analysed for collagen formation and NF-κB p50 transactivation. Treatment with CLA isomers but not LA significantly reduced PDGF-stimulated [3H] proline incorporation into cell layer protein of SMCs without altering cell proliferation. Simultaneous treatment with the PPARγ inhibitor T0070907 abrogated this effect. Treatment of SMCs with c9t11-CLA and t10c12-CLA significantly reduced PDGF-induced NF-κB p50 activation. CLA isomers inhibit PDGF-stimulated collagen production by vascular SMCs, which is considered to be a hallmark of atherosclerosis, in a PPARγ-dependent manner. Whether inhibition of the NF-κB-pathway is of significance for the reduction of collagen formation by CLA isomers needs further investigation.
         datePublished:2008-02-09T00:00:00Z
         dateModified:2008-02-09T00:00:00Z
         pageStart:59
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      headline:Conjugated linoleic acid isomers inhibit platelet-derived growth factor-induced NF-κB transactivation and collagen formation in human vascular smooth muscle cells
      description:Atherosclerosis is characterized by extensive thickening of the arterial intima partially resulting from deposition of collagen by vascular smooth muscle cells (SMCs). Polyunsaturated fatty acids stimulate collagen formation through NF-κB activation. The present study aimed to explore the effect of conjugated linoleic acids (CLAs) which are known to inhibit NF-κB activation on collagen formation by SMCs. Vascular SMCs were cultured with 50 µmol/l of CLA isomers (c9t11-CLA, t10c12-CLA) or linoleic acid (LA) and analysed for collagen formation and NF-κB p50 transactivation. Treatment with CLA isomers but not LA significantly reduced PDGF-stimulated [3H] proline incorporation into cell layer protein of SMCs without altering cell proliferation. Simultaneous treatment with the PPARγ inhibitor T0070907 abrogated this effect. Treatment of SMCs with c9t11-CLA and t10c12-CLA significantly reduced PDGF-induced NF-κB p50 activation. CLA isomers inhibit PDGF-stimulated collagen production by vascular SMCs, which is considered to be a hallmark of atherosclerosis, in a PPARγ-dependent manner. Whether inhibition of the NF-κB-pathway is of significance for the reduction of collagen formation by CLA isomers needs further investigation.
      datePublished:2008-02-09T00:00:00Z
      dateModified:2008-02-09T00:00:00Z
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         Nutrition
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