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(Circulation Research. 2007;100:e81.)
© 2007 American Heart Association, Inc.

Letter to the Editor

Triglyceride-Rich Lipoproteins From Normotrygliceridemic Subjects and Hyperlipidemic Patients Differently Affect Endothelial Cell Activation and Gene Expression Patterns

Giuseppe D. Norata, Alberico L. Catapano

Centro SISA per lo Studio della Aterosclerosi, Ospedale Bassini, Cinisello Balsamo, Milano Department of Pharmacological Sciences, University of Milan Italy

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We read with interest the article by Ting et al¹ showing that post-prandial triglyceride-rich lipoproteins (PP-TGRL) from healthy human volunteers (NTG) fail to promote endothelial inflammation but increase the tumor necrosis factor- response of endothelial cells. We would like to add further information on this topic recently obtained in our laboratory^2,3 that may contribute to the understanding of the role of TG-rich lipoproteins in modulating endothelial function(s).

Ting et al, showed that PP-TGRL are unable to elicit pro-inflammatory responses and this finding is based on the lack of effect of PP-TGRL on ICAM-1, VCAM-1 and E-selectin mRNA expression. An observation confirmed by the lack of monocyte recruitment by endothelial cells exposed to PP-TGRL. However, and consistent with our findings,^2,3 postprandial TGRL per se activated p38MAPK a key pathway of intracellular signaling in inflammation.

In addition we showed that postprandial TGRL from type IV hyperlipidemic patients induce to a larger extent, compared with fasting TGRL, phosphorylation of p38 MAPK, CREB and IKB- in human endothelial cells and increase the DNA binding activity of CREB, NFAT and NF-kB.³ These results prompted us to investigate the differences between PP-TGRL form NTG subjects and HTG patients on endothelial cell gene expression.^2,4,5 We observed the induction by PP-TGRL form HTG patients but not by NTG subjects of a large set of proinflammatory genes including VCAM-1, PECAM-1, ELAM-1, ICAM-1, P-selectin, MCP-1, IL-6, TLR-4, CD40, ADAMTS1 and PAI-1. Furthermore, in vivo, the endothelium-dependent flow mediated dilatation (FMD) decreased in both NTG and HTG subjects . . . [Full Text of this Article]