Expression of the peroxisome proliferator-activated receptor gamma (PPARgamma) in human atherosclerosis and regulation in macrophages by colony stimulating factors and oxidized low density lipoprotein.

Détails

ID Serval
serval:BIB_1EFDA6B0CDCF
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Expression of the peroxisome proliferator-activated receptor gamma (PPARgamma) in human atherosclerosis and regulation in macrophages by colony stimulating factors and oxidized low density lipoprotein.
Périodique
Proceedings of the National Academy of Sciences of the United States of America
Auteur(s)
Ricote M., Huang J., Fajas L., Li A., Welch J., Najib J., Witztum J.L., Auwerx J., Palinski W., Glass C.K.
ISSN
0027-8424 (Print)
ISSN-L
0027-8424
Statut éditorial
Publié
Date de publication
1998
Volume
95
Numéro
13
Pages
7614-7619
Langue
anglais
Résumé
The peroxisome proliferator-activated receptor gamma (PPARgamma) is a ligand-dependent transcription factor that has been demonstrated to regulate fat cell development and glucose homeostasis. PPARgamma is also expressed in a subset of macrophages and negatively regulates the expression of several proinflammatory genes in response to natural and synthetic ligands. We here demonstrate that PPARgamma is expressed in macrophage foam cells of human atherosclerotic lesions, in a pattern that is highly correlated with that of oxidation-specific epitopes. Oxidized low density lipoprotein (oxLDL) and macrophage colony-stimulating factor, which are known to be present in atherosclerotic lesions, stimulated PPARgamma expression in primary macrophages and monocytic cell lines. PPARgamma mRNA expression was also induced in primary macrophages and THP-1 monocytic leukemia cells by the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA). Inhibition of protein kinase C blocked the induction of PPARgamma expression by TPA, but not by oxLDL, suggesting that more than one signaling pathway regulates PPARgamma expression in macrophages. TPA induced the expression of PPARgamma in RAW 264.7 macrophages by increasing transcription from the PPARgamma1 and PPARgamma3 promoters. In concert, these observations provide insights into the regulation of PPARgamma expression in activated macrophages and raise the possibility that PPARgamma ligands may influence the progression of atherosclerosis.
Mots-clé
Animals, Arteriosclerosis/metabolism, Cell Differentiation, Cells, Cultured, Colony-Stimulating Factors/metabolism, Foam Cells/drug effects, Foam Cells/metabolism, Humans, Lipoproteins, LDL/metabolism, Mice, Promoter Regions, Genetic, Protein Kinase C/antagonists & inhibitors, Receptors, Cytoplasmic and Nuclear/biosynthesis, Tetradecanoylphorbol Acetate/pharmacology, Transcription Factors/biosynthesis
Pubmed
Web of science
Open Access
Oui
Création de la notice
07/03/2013 17:11
Dernière modification de la notice
08/05/2019 15:29
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