title: Tripeptides from dietary proteins inhibit TNFalpha-induced monocyte adhesion to human aortic endothelial cells.
abstract: Dietary proteins have been shown to reduce atherosclerosis development. Although the components of proteins responsible for this effect are largely unknown, it has been suggested that specific bioactive peptides are involved. In order to elucidate possible atheroprotective mechanisms of bioactive peptides, we evaluated the effect of different tripeptides derived from food proteins on leukocyte-endothelial cell interaction which is regarded as a key event in atherosclerosis development. Treatment of human aortic endothelial cells (HAEC) with 50 microM of Val-Pro-Leu, Ser-Ser-Ser and Glu-Glu-Glu inhibited TNFalpha-induced monocyte adhesion and expression of the adhesion molecule E-selectin (P<0.05). Expression of intercellular adhesion molecule-1 was not influenced by the tripeptides tested in TNFalpha-treated HAEC, whereas expression of vascular cell adhesion molecule-1 was only influenced by Ser-Ser-Ser (P<0.05). Treatment with 50 microM of Ser-Ser-Ser and Glu-Glu-Glu, but not Val-Pro-Leu caused an inhibition of TNFalpha-induced activation of NF-kappaB compared to control cells (P<0.05). In conclusion, the present study shows that short peptides derived from food proteins reduce monocyte adhesion to HAEC. Since monocyte adhesion to the endothelium is a crucial step in the early phase of atherosclerosis, inhibition of monocyte adhesion by bioactive peptides might be one plausible mechanism explaining amelioration of atherosclerotic lesion development by dietary proteins.
authors.affiliation: Institute of Agricultural and Nutritional Sciences, Martin-Luther-University of Halle-Wittenberg, Von-Danckelmann-Platz 2, D-06120 Halle (Saale), Germany. robert.ringseis@landw.uni-halle.de
authors.forename: Robert
authors.initials: R
authors.lastname: Ringseis
authors.forename: Vera
authors.initials: V
authors.lastname: Götze
authors.forename: Klaus
authors.initials: K
authors.lastname: Eder
mesh_terms: D000328:Adult; D001011:Aorta / Q000166:cytology; D002448:Cell Adhesion / Q000187:drug effects / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000032:analysis / Q000096:biosynthesis*; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D004044:Dietary Proteins / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D019040:E-Selectin / Q000096:biosynthesis; D042783:Endothelial Cells / Q000166:cytology / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000166:cytology; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D009000:Monocytes / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D009842:Oligopeptides / Q000494:pharmacology*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis
chemical_list: D015815:Cell Adhesion Molecules; D004044:Dietary Proteins; D019040:E-Selectin; D009842:Oligopeptides; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1