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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Main Authors: Lamers, Daniela, Schlich, Raphaela, Greulich, Sabrina, Sasson, Shlomo, Sell, Henrike, Eckel, Jürgen
Format: Online
Language:English
Published: Blackwell Publishing Ltd 2011
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3822630/
id pubmed-3822630
recordtype oai_dc
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 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
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Lamers, Daniela
Schlich, Raphaela
Greulich, Sabrina
Sasson, Shlomo
Sell, Henrike
Eckel, Jürgen
spellingShingle 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
author_facet Lamers, Daniela
Schlich, Raphaela
Greulich, Sabrina
Sasson, Shlomo
Sell, Henrike
Eckel, Jürgen
author_sort Lamers, Daniela
title 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_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_sort oleic acid and adipokines synergize in inducing proliferation and inflammatory signalling in human vascular smooth muscle cells
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.
publisher Blackwell Publishing Ltd
publishDate 2011
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3822630/
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