Influence of (n-3) Fatty Acids on Platelets and Endothelial Cells

The asymmetric distribution of phospholipids in bovine endothelial-cell membranes was probed with 2,4,6-trinitrobenzenesulphonate and purified phospholipase A2. The data suggest that phosphotidylethanolamine is primarily located in the inner lipid bilayer, as reported for other cell types. Stearic acid is taken up by the endothelial cells and is randomly distributed among the membrane phospholipids. In contrast, the polyunsaturated fatty acids (arachidonic, eicosatrienoic and eicosapentaenoic acids) have initial incorporation into the phosphatidylcholine fraction. These fatty acids then undergo a time-dependent transfer from phosphatidylcholine to phosphatidylethanolamine. Thus we propose that endothelial cells possess a mechanism for the selective internalization of polyunsaturated fatty acids.

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Serum from preeclamptic women induces vascular cell adhesion molecule-1 expression on human endothelial cells in vitro: A possible role of increased circulating levels of free fatty acids

American Journal of Obstetrics and Gynecology ◽

10.1016/s0002-9378(98)70061-4 ◽

1998 ◽

Vol 179 (3) ◽

pp. 665-670 ◽

Cited By ~ 19

Author(s):

Marit J.R. Endresen ◽

Jonathan M. Morris ◽

Ariadne C. Nobrega ◽

Davina Buckley ◽

Elizabeth A. Linton ◽

...

Keyword(s):

Fatty Acids ◽

Endothelial Cells ◽

Cell Adhesion Molecule ◽

Vascular Cell Adhesion ◽

Human Endothelial Cells ◽

Vascular Cell ◽

Cell Adhesion Molecule 1 ◽

Circulating Levels

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Turnover of eicosanoid precursor fatty acids among phospholipid classes and subclasses of cultured human umbilical vein endothelial cells

Biochemical Journal ◽

10.1042/bj2580427 ◽

1989 ◽

Vol 258 (2) ◽

pp. 427-434 ◽

Cited By ~ 22

Author(s):

H Takayama ◽

M H Kroll ◽

M A Gimbrone ◽

A I Schafer

Keyword(s):

Fatty Acids ◽

Endothelial Cells ◽

Umbilical Vein ◽

Ionophore A23187 ◽

Human Umbilical Vein ◽

Phospholipid Classes ◽

Specific Increase ◽

Umbilical Vein Endothelial Cells ◽

Relationship Of ◽

The Relationship

Using cultured human umbilical vein endothelial cells, in which phosphatidylcholine (PC) is equally pulse-labelled by various eicosanoid precursor fatty acids (EPFAs), we have studied the remodelling of EPFAs among the phospholipid classes and subclasses with and without activation, and the relationship of this remodelling process to the selective release of arachidonic acid (AA) by phospholipase A2-mediated cell stimulation. When endothelial cells are pulse-incubated with radiolabelled EPFA for 15 min, greater than 80% of cell-associated radioactivity is present in phospholipids, among which greater than 60% is found in 1,2-diacyl-sn-glycero-3-phosphocholine (diacyl PC). After removing unincorporated radioactivity, reincubation of the pulse-labelled cells for up to 6 h results in progressive decrease in EPFA-labelled diacyl PC, increase in AA- or eicosapentaenoic acid (EPA)-labelled 1-O-alk-1-enyl-2-acyl-sn-glycero-3-phosphoethanolamine (plasmalogen PE) and increase only in AA-labelled 1-O-alkyl-2-acyl-sn-glycero-3-phosphocholine (alkyl PC). This redistribution of radiolabelled phospholipids is not altered by the presence of excess non-radiolabelled EPFAs. When aspirin-treated EPFA-labelled endothelial cells are stimulated with ionophore A23187, a very selective release of AA is noted in comparison with eicosatrienoate (ETA) or EPA, accompanied by an equivalent decrease in AA-labelled diacyl PC and specific increase in AA-labelled plasmalogen PE and alkyl PC. These selective changes in AA radioactivity induced by A23187 are enhanced 2-fold by pretreating the AA-labelled cells with phorbol 12-myristate 13-acetate, which by itself induces no changes. The changes in radioactivity induced by A23187 without and with phorbol ester among the released AA, the diacyl PC and the plasmalogen PE are significantly correlated with each other. These results indicate that human endothelial cells incorporate EPFAs (AA, ETA, EPA) equally into diacyl PC but selectively release AA esterified into diacyl PC with specific remodelling into plasmalogen PE and alkyl PC.

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Trans Fatty Acids: Induction of a Pro-inflammatory Phenotype in Endothelial Cells

Lipids ◽

10.1007/s11745-012-3681-2 ◽

2012 ◽

Vol 47 (7) ◽

pp. 647-657 ◽

Cited By ~ 23

Author(s):

Kevin A. Harvey ◽

Candace L. Walker ◽

Zhidong Xu ◽

Phillip Whitley ◽

Rafat A. Siddiqui

Keyword(s):

Fatty Acids ◽

Endothelial Cells ◽

Trans Fatty Acids ◽

Inflammatory Phenotype

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Real- time interaction analysis of Shiga toxins and membrane microdomains of primary human brain microvascular endothelial cells

Glycobiology ◽

10.1093/glycob/cwz091 ◽

2019 ◽

Cited By ~ 2

Author(s):

Johanna Detzner ◽

Daniel Steil ◽

Gottfried Pohlentz ◽

Nadine Legros ◽

Hans-Ulrich Humpf ◽

...

Keyword(s):

Fatty Acids ◽

Endothelial Cells ◽

Human Brain ◽

Real Time ◽

Interaction Analysis ◽

Microvascular Endothelial Cells ◽

Brain Microvascular Endothelial Cells ◽

Membrane Phase ◽

Shiga Toxins ◽

Microvascular Endothelial

Abstract Infections of the human intestinal tract with enterohemorrhagic Escherichia coli (EHEC) result in massive extraintestinal complications due to translocation of EHEC-released Shiga toxins (Stxs) from the gut into the circulation. Stx-mediated damage of the cerebral microvasculature raises serious brain dysfunction being the most frequent cause of acute mortality in patients suffering from severe EHEC infections. Stx2a and Stx2e are associated with heavy and mild course of infection, respectively. Stx2a preferentially binds to globotriaosylceramide (Gb3Cer, Galα1-4Galβ1-4Glcβ1-1Cer), while Stx2e prefers globotetraosylceramide (Gb4Cer, GalNAcβ1-3Galα1-4Galβ1-4Glcβ1-1Cer). Both glycosphingolipids (GSLs) were detected in detergent-resistant membranes (DRMs) of primary human brain microvascular endothelial cells (pHBMECs) resembling microdomains of the plasma membrane. In this study we show that Gb3Cer and Gb4Cer of pHBMECs with saturated C16:0, C22:0, and C24:0 fatty acids dominated in DRMs, corresponding to the liquid-ordered membrane phase, whereas lipoforms carrying unsaturated C24:1 and C24:2 fatty acids prevailed in the nonDRM fractions, which correspond to the liquid-disordered membrane phase. Similarly, a shift of the phospholipids from saturated lipoforms in the DRM to unsaturated species in the nonDRM fractions was observed. Real-time biomolecular interaction analysis using affinity-purified Stx2a and Stx2e, recorded with a surface acoustic wave (SAW) biosensor, evidenced high binding strength of both toxins towards DRMs and failure in interaction with nonDRMs. These results support the hypothesis of preferential binding of Stxs towards microdomains harbouring GSL receptors carrying saturated fatty acids in their lipid anchors. Collectively, unravelling the precise mechanisms of Stx-microdomain interaction may help to develop antiadhesive compounds to combat Stx-mediated cellular injury.

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