Milk-derived bioactive peptides inhibit human endothelial-monocyte interactions via PPAR-¿ dependent regulation of NF-¿B

Hdl Handle:
http://hdl.handle.net/10147/560476
Title:
Milk-derived bioactive peptides inhibit human endothelial-monocyte interactions via PPAR-¿ dependent regulation of NF-¿B
Authors:
Marcone, Simone; Haughton, Karen; Simpson, Paul J; Belton, Orina; Fitzgerald, Desmond J
Citation:
Journal of Inflammation. 2015 Jan 20;12(1):1
Issue Date:
20-Jan-2015
URI:
http://dx.doi.org/10.1186/s12950-014-0044-1; http://hdl.handle.net/10147/560476
Abstract:
Abstract Background Milk-derived bioactive peptides retain many biological properties and have therapeutic effects in cardiovascular disorders such as atherosclerosis. Under inflammatory conditions the expression of endothelial cells adhesion molecules is induced, increasing monocyte adhesion to human vessel wall, a critical step in the pathogenesis of atherosclerosis. In the present work we explored the effects of milk-derived bioactive peptides on the expression of the inflammatory phenotype of human endothelial cells and their effects on monocyte adherence to endothelial cells. Results Treatment of endothelial cells with milk-derived hydrolysate inhibited their production of inflammatory proteins MCP-1 and IL-8 and expression of VCAM-1, ICAM-1 and E-selectin. Milk derived hydrolysate also attenuated the adhesion of human monocytes to activated endothelial cells. The effect was similar to that obtained in endothelial cells treated with troglitazone, a ligand of peroxisome proliferators-activator receptor-gamma (PPAR-γ). PPAR-γ is a transcription factor which when activated antagonises the pro-inflammatory capability of nuclear factor κB (NF-κB). We further examined whether the effects of milk-derived hydrolysates on endothelial cells may be mediated through NF-κB activation via a PPAR-γ dependent mechanism. The specific PPAR-γ inhibitor, GW9662 blocked the effects of the hydrolysate on the NF-κB-mediated chemokines and adhesion molecules expression in endothelial cells. Conclusions These results suggest that milk-derived bioactive peptides work as anti-atherogenic agents through the inhibition of endothelial-dependent adhesive interactions with monocytes by inhibiting the NF-κB pathway through a PPAR-γ dependent mechanism.
Language:
en
Keywords:
ATHEROSCLEROSIS; INFLAMMATION

Full metadata record

DC FieldValue Language
dc.contributor.authorMarcone, Simoneen
dc.contributor.authorHaughton, Karenen
dc.contributor.authorSimpson, Paul Jen
dc.contributor.authorBelton, Orinaen
dc.contributor.authorFitzgerald, Desmond Jen
dc.date.accessioned2015-07-15T09:31:32Zen
dc.date.available2015-07-15T09:31:32Zen
dc.date.issued2015-01-20en
dc.identifier.citationJournal of Inflammation. 2015 Jan 20;12(1):1en
dc.identifier.urihttp://dx.doi.org/10.1186/s12950-014-0044-1en
dc.identifier.urihttp://hdl.handle.net/10147/560476en
dc.description.abstractAbstract Background Milk-derived bioactive peptides retain many biological properties and have therapeutic effects in cardiovascular disorders such as atherosclerosis. Under inflammatory conditions the expression of endothelial cells adhesion molecules is induced, increasing monocyte adhesion to human vessel wall, a critical step in the pathogenesis of atherosclerosis. In the present work we explored the effects of milk-derived bioactive peptides on the expression of the inflammatory phenotype of human endothelial cells and their effects on monocyte adherence to endothelial cells. Results Treatment of endothelial cells with milk-derived hydrolysate inhibited their production of inflammatory proteins MCP-1 and IL-8 and expression of VCAM-1, ICAM-1 and E-selectin. Milk derived hydrolysate also attenuated the adhesion of human monocytes to activated endothelial cells. The effect was similar to that obtained in endothelial cells treated with troglitazone, a ligand of peroxisome proliferators-activator receptor-gamma (PPAR-γ). PPAR-γ is a transcription factor which when activated antagonises the pro-inflammatory capability of nuclear factor κB (NF-κB). We further examined whether the effects of milk-derived hydrolysates on endothelial cells may be mediated through NF-κB activation via a PPAR-γ dependent mechanism. The specific PPAR-γ inhibitor, GW9662 blocked the effects of the hydrolysate on the NF-κB-mediated chemokines and adhesion molecules expression in endothelial cells. Conclusions These results suggest that milk-derived bioactive peptides work as anti-atherogenic agents through the inhibition of endothelial-dependent adhesive interactions with monocytes by inhibiting the NF-κB pathway through a PPAR-γ dependent mechanism.-
dc.language.isoenen
dc.subjectATHEROSCLEROSISen
dc.subjectINFLAMMATIONen
dc.titleMilk-derived bioactive peptides inhibit human endothelial-monocyte interactions via PPAR-¿ dependent regulation of NF-¿Ben
dc.language.rfc3066en-
dc.rights.holderSimone Marcone et al.; licensee BioMed Central Ltd.-
dc.description.statusPeer Reviewed-
dc.date.updated2015-01-27T20:04:10Z-
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