PMID- 11821020
OWN - NLM
STAT- MEDLINE
DCOM- 20020327
LR  - 20190624
IS  - 0014-2999 (Print)
IS  - 0014-2999 (Linking)
VI  - 435
IP  - 2-3
DP  - 2002 Jan 25
TI  - PPARalpha and PPARdelta activators inhibit cytokine-induced nuclear translocation 
      of NF-kappaB and expression of VCAM-1 in EAhy926 endothelial cells.
PG  - 143-51
AB  - Endothelium injury is a primary event in atherogenesis, which is followed by 
      monocyte infiltration, macrophage differentiation, and smooth muscle cell 
      migration. Peroxisome proliferator-activated receptors (PPARs) are transcription 
      factors now recognized as important mediators in the inflammatory response. The 
      aim of this study was to develop a human endothelial model to evaluate 
      anti-inflammatory properties of PPAR activators. PPAR proteins (alpha, delta and 
      gamma) are expressed in EAhy926 endothelial cells (ECs). Pirinixic acid 
      (Wy-14643), fenofibrate, fenofibric acid, the Merck ligand PPARdelta activator 
      L-165041, 15-deoxy-Delta(12,14)-prostaglandin J2, but not rosiglitazone 
      (BRL-49653) inhibited the induced expression of vascular cell adhesion molecule-1 
      (VCAM-1), as measured by enzyme linked immunosorbent assay (ELISA), and monocyte 
      binding to activated-EAhy926 cells. The PPARdelta activator L-165041 had the 
      greatest potency to reduce cytokine-induced monocyte chemotactic protein-1 
      (MCP-1) secretion. All PPAR activators tested which impaired VCAM-1 expression 
      reduced significantly nuclear p65 amount. These results show that EAhy926 
      endothelial cells are an adequate tool to substantiate and characterize 
      inflammatory impacts of PPAR activators.
FAU - Rival, Yves
AU  - Rival Y
AD  - Centre de Recherche Pierre Fabre, 17 Avenue Jean Moulin, 81106 Cedex, Castres, 
      France. yves.rival@pierre-fabre.com
FAU - Beneteau, Nathalie
AU  - Beneteau N
FAU - Taillandier, Thierry
AU  - Taillandier T
FAU - Pezet, Mylene
AU  - Pezet M
FAU - Dupont-Passelaigue, Elisabeth
AU  - Dupont-Passelaigue E
FAU - Patoiseau, Jean Francois
AU  - Patoiseau JF
FAU - Junquero, Didier
AU  - Junquero D
FAU - Colpaert, Francis C
AU  - Colpaert FC
FAU - Delhon, Andre
AU  - Delhon A
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - Eur J Pharmacol
JT  - European journal of pharmacology
JID - 1254354
RN  - 0 (4-(3-(2-propyl-3-hydroxy-4-acetyl)phenoxy)propyloxyphenoxy acetic acid)
RN  - 0 (Acetates)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (NF-kappa B)
RN  - 0 (Peroxisome Proliferators)
RN  - 0 (Phenols)
RN  - 0 (Phenoxyacetates)
RN  - 0 (Pyrimidines)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Transcription Factors)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 86C4MRT55A (pirinixic acid)
SB  - IM
MH  - Acetates/*pharmacology
MH  - Active Transport, Cell Nucleus
MH  - Binding Sites
MH  - Cell Nucleus/drug effects/metabolism
MH  - Cells, Cultured
MH  - Chemokine CCL2/metabolism
MH  - Cytokines/metabolism
MH  - Down-Regulation/drug effects
MH  - Endothelium, Vascular/*drug effects/metabolism
MH  - Gene Expression/drug effects
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/metabolism
MH  - Monocytes/drug effects/metabolism
MH  - NF-kappa B/*metabolism
MH  - Peroxisome Proliferators/*pharmacology
MH  - Phenols/*pharmacology
MH  - Phenoxyacetates
MH  - Pyrimidines/*pharmacology
MH  - Receptors, Cytoplasmic and Nuclear/*metabolism
MH  - Signal Transduction/drug effects/physiology
MH  - Transcription Factors/*metabolism
MH  - Vascular Cell Adhesion Molecule-1/*biosynthesis
EDAT- 2002/02/01 10:00
MHDA- 2002/03/28 10:01
CRDT- 2002/02/01 10:00
PHST- 2002/02/01 10:00 [pubmed]
PHST- 2002/03/28 10:01 [medline]
PHST- 2002/02/01 10:00 [entrez]
AID - S0014299901015898 [pii]
AID - 10.1016/s0014-2999(01)01589-8 [doi]
PST - ppublish
SO  - Eur J Pharmacol. 2002 Jan 25;435(2-3):143-51. doi: 10.1016/s0014-2999(01)01589-8.