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Oleic acid and adipokines synergize in inducing proliferation and inflammatory signalling in human vascular smooth muscle cells

In the context of obesity, perivascular fat produces various adipokines and releases free fatty acids, which may induce inflammation and proliferation in the vascular wall. In this study we investigated how adipokines, oleic acid (OA) and the combined treatment regulate human vascular smooth muscle...

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Autores principales: Lamers, Daniela, Schlich, Raphaela, Greulich, Sabrina, Sasson, Shlomo, Sell, Henrike, Eckel, Jürgen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3822630/
https://www.ncbi.nlm.nih.gov/pubmed/20518853
http://dx.doi.org/10.1111/j.1582-4934.2010.01099.x
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author Lamers, Daniela
Schlich, Raphaela
Greulich, Sabrina
Sasson, Shlomo
Sell, Henrike
Eckel, Jürgen
author_facet Lamers, Daniela
Schlich, Raphaela
Greulich, Sabrina
Sasson, Shlomo
Sell, Henrike
Eckel, Jürgen
author_sort Lamers, Daniela
collection PubMed
description In the context of obesity, perivascular fat produces various adipokines and releases free fatty acids, which may induce inflammation and proliferation in the vascular wall. In this study we investigated how adipokines, oleic acid (OA) and the combined treatment regulate human vascular smooth muscle cell (hVSMC) proliferation and migration and the underlying signalling pathways. Adipocyte-conditioned media (CM) generated from human adipocytes induces a prominent proliferation and migration of hVSMC. Autocrine action of adiponectin totally abolishes CM-induced proliferation. Furthermore, OA but not palmitic acid induces proliferation of hVSMC. CM itself does not contain fatty acids, but CM in combination with OA markedly enhances proliferation of hVSMC in a synergistic way. Both the nuclear factor (NF)-κB and the mammalian target of rapamycin (mTOR) pathway were synergistically activated under these conditions and found to be essential for hVSMC proliferation. Expression of iNOS and production of nitric oxide was only enhanced by combined treatment inducing a marked release of VEGF. Combination of OA and VEGF induces an additive increase of hVSMC proliferation. We could show that the combination of CM and OA led to a synergistic proliferation of hVSMC. Expression of iNOS and production of nitric oxide were only enhanced under these conditions and were paralleled by a marked release of VEGF. These results suggest that the combined elevated release of fatty acids and adipokines by adipose tissue in obesity might be critically related to hVSMC dysfunction, vascular inflammation and the development of atherosclerosis.
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spelling pubmed-38226302015-04-06 Oleic acid and adipokines synergize in inducing proliferation and inflammatory signalling in human vascular smooth muscle cells Lamers, Daniela Schlich, Raphaela Greulich, Sabrina Sasson, Shlomo Sell, Henrike Eckel, Jürgen J Cell Mol Med Articles In the context of obesity, perivascular fat produces various adipokines and releases free fatty acids, which may induce inflammation and proliferation in the vascular wall. In this study we investigated how adipokines, oleic acid (OA) and the combined treatment regulate human vascular smooth muscle cell (hVSMC) proliferation and migration and the underlying signalling pathways. Adipocyte-conditioned media (CM) generated from human adipocytes induces a prominent proliferation and migration of hVSMC. Autocrine action of adiponectin totally abolishes CM-induced proliferation. Furthermore, OA but not palmitic acid induces proliferation of hVSMC. CM itself does not contain fatty acids, but CM in combination with OA markedly enhances proliferation of hVSMC in a synergistic way. Both the nuclear factor (NF)-κB and the mammalian target of rapamycin (mTOR) pathway were synergistically activated under these conditions and found to be essential for hVSMC proliferation. Expression of iNOS and production of nitric oxide was only enhanced by combined treatment inducing a marked release of VEGF. Combination of OA and VEGF induces an additive increase of hVSMC proliferation. We could show that the combination of CM and OA led to a synergistic proliferation of hVSMC. Expression of iNOS and production of nitric oxide were only enhanced under these conditions and were paralleled by a marked release of VEGF. These results suggest that the combined elevated release of fatty acids and adipokines by adipose tissue in obesity might be critically related to hVSMC dysfunction, vascular inflammation and the development of atherosclerosis. Blackwell Publishing Ltd 2011-05 2010-06-01 /pmc/articles/PMC3822630/ /pubmed/20518853 http://dx.doi.org/10.1111/j.1582-4934.2010.01099.x Text en © 2011 The Authors Journal of Cellular and Molecular Medicine © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd
spellingShingle Articles
Lamers, Daniela
Schlich, Raphaela
Greulich, Sabrina
Sasson, Shlomo
Sell, Henrike
Eckel, Jürgen
Oleic acid and adipokines synergize in inducing proliferation and inflammatory signalling in human vascular smooth muscle cells
title Oleic acid and adipokines synergize in inducing proliferation and inflammatory signalling in human vascular smooth muscle cells
title_full Oleic acid and adipokines synergize in inducing proliferation and inflammatory signalling in human vascular smooth muscle cells
title_fullStr Oleic acid and adipokines synergize in inducing proliferation and inflammatory signalling in human vascular smooth muscle cells
title_full_unstemmed Oleic acid and adipokines synergize in inducing proliferation and inflammatory signalling in human vascular smooth muscle cells
title_short Oleic acid and adipokines synergize in inducing proliferation and inflammatory signalling in human vascular smooth muscle cells
title_sort oleic acid and adipokines synergize in inducing proliferation and inflammatory signalling in human vascular smooth muscle cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3822630/
https://www.ncbi.nlm.nih.gov/pubmed/20518853
http://dx.doi.org/10.1111/j.1582-4934.2010.01099.x
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