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Cardiovascular Research Advance Access originally published online on March 21, 2008
Cardiovascular Research 2008 79(2):294-303; doi:10.1093/cvr/cvn082
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Influence of postprandial triglyceride-rich lipoproteins on lipid-mediated gene expression in smooth muscle cells of the human coronary artery

Beatriz Bermúdez1,{dagger}, Sergio López1,{dagger}, Yolanda M. Pacheco1, José Villar2, Francisco J.G. Muriana1, Jöerg D. Hoheisel3, Andrea Bauer3 and Rocío Abia1,*

1 Cellular and Molecular Nutrition, Instituto de la Grasa (CSIC), Avda. Padre García Tejero, 4, 41012 Seville, Spain
2 Service of Internal Medicine, Hospitales Universitarios Virgen del Rocío, Seville, Spain
3 Department of Functional Genome Analysis, German Cancer Research Center, Heidelberg, Germany

* Corresponding author. Tel: +34 954 611550; fax: +34 954 616790. E-mail address: abia{at}ig.csic.es

Aims: Postprandial triglyceride-rich lipoproteins (TRL) have a direct effect on vascular smooth muscle cells (SMC) and they increase the risk of atherogenesis. Here, we have tested the hypothesis that the different fatty acid composition of TRL is capable of differentially modifying gene expression in human coronary artery SMC (CASMC). In addition, the effect of TRL on cell proliferation and transcription factor activation was also evaluated.

Methods and results: TRL were prepared from plasma of healthy volunteers after the ingestion of meals enriched in refined olive oil (ROO), butter or a mixture of vegetable and fish oils (VEFO). We use cDNA microarrays to determine the genes differentially expressed in TRL-treated CASMC. Correspondence cluster analysis demonstrated that TRL-butter, -ROO and -VEFO provoked different transcriptional profiles in CASMC. Sixty-six genes were regulated by TRL-butter, 55 by –ROO, and 47 by -VEFO. The data revealed that TRL-butter predominantly activated genes involved in the regulation of cell proliferation and inflammation. Likewise, TRL-VEFO induced the expression of genes implicated in inflammation, while TRL-ROO promoted a less atherogenic gene profile.

Conclusion: The pathophysiological contribution of TRL to the development of atherosclerosis and the stability of atherosclerotic plaques may depend on the fatty acid composition of TRL. Our findings suggest a role for macrophage-inhibiting cytokine-1 (MIC-1) in coronary artery cardiovascular events.

KEYWORDS Postprandial lipoproteins; Gene array analysis; Coronary disease; Fatty acids; Smooth muscle cells

Time for primary review: 27 days

{dagger} B.B. and S.L. contributed equally to this work.


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