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Transcriptional Repression of Atherogenic Inflammation: Modulation by PPAR
Chih-Hao Lee,1
Ajay Chawla,1*
Ned Urbiztondo,1
Debbie Liao,1
William A. Boisvert,2
Ronald M. Evans1
Abstract:
The formation of an atherosclerotic lesion is mediated by lipid-ladenmacrophages (foam cells), which also establish chronic inflammationassociated with lesion progression. The peroxisome proliferator-activatedreceptor (PPAR) promotes lipid uptake and efflux in these atherogeniccells. In contrast, we found that the closely related receptorPPAR controls the inflammatory status of the macrophage. Deletionof PPAR from foam cells increased the availability of inflammatorysuppressors, which in turn reduced atherosclerotic lesion areaby more than 50%. We propose an unconventional ligand-dependenttranscriptional pathway in which PPAR controls an inflammatoryswitch through its association and disassociation with transcriptionalrepressors. PPAR and its ligands may thus serve as therapeutictargets to attenuate inflammation and slow the progression ofatherosclerosis.
1 Howard Hughes Medical Institute, Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. 2 Vascular Medicine Research, Brigham & Women's Hospital, 65 Landsdowne Street, Room 275, Cambridge, MA 02139, USA.
AMPK{alpha}2 exerts its anti-inflammatory effects through PARP-1 and Bcl-6.
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PNAS
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A Nuclear Receptor Atlas: Macrophage Activation.
G. D. Barish, M. Downes, W. A. Alaynick, R. T. Yu, C. B. Ocampo, A. L. Bookout, D. J. Mangelsdorf, and R. M. Evans (2005)
Mol. Endocrinol.
19, 2466-2477
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Proteomic and Transcriptomic Analyses of Macrophages with an Increased Resistance to Oxidized Low Density Lipoprotein (oxLDL)-induced Cytotoxicity Generated by Chronic Exposure to oxLDL.
Prostacyclin signaling in the kidney: implications for health and disease.
R. Nasrallah and R. L. Hebert (2005)
Am J Physiol Renal Physiol
289, F235-F246
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Peroxisome Proliferator-Activated Receptor {beta}/{delta} Exerts a Strong Protection from Ischemic Acute Renal Failure.
E. Letavernier, J. Perez, E. Joye, A. Bellocq, B. Fouqueray, J.-P. Haymann, D. Heudes, W. Wahli, B. Desvergne, and L. Baud (2005)
J. Am. Soc. Nephrol.
16, 2395-2402
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Antiinflammatory Effects of Tetradecylthioacetic Acid Involve Both Peroxisome Proliferator-Activated Receptor {alpha}-Dependent and -Independent Pathways.
E. Dyroy, A. Yndestad, T. Ueland, B. Halvorsen, J. K. Damas, P. Aukrust, and R. K. Berge (2005)
Arterioscler Thromb Vasc Biol
25, 1364-1369
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Modulation of Peroxisome Proliferator-Activated Receptor {delta} Activity Affects Neural Cell Adhesion Molecule and Polysialyltransferase ST8SiaIV Induction by Teratogenic Valproic Acid Analogs in F9 Cell Differentiation.
Peroxisome Proliferator-Activated Receptor {delta} and {gamma} Agonists Differentially Alter Tumor Differentiation and Progression during Mammary Carcinogenesis.
Y. Yin, R. G. Russell, L. E. Dettin, R. Bai, Z.-L. Wei, A. P. Kozikowski, L. Kopleovich, and R. I. Glazer (2005)
Cancer Res.
65, 3950-3957
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Effects of peroxisome proliferator-activated receptor {alpha}/{delta} agonists on HDL-cholesterol in vervet monkeys.
J. M. Wallace, M. Schwarz, P. Coward, J. Houze, J. K. Sawyer, K. L. Kelley, A. Chai, and L. L. Rudel (2005)
J. Lipid Res.
46, 1009-1016
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Dehydroepiandrosterone Can Inhibit the Proliferation of Myeloma Cells and the Interleukin-6 Production of Bone Marrow Mononuclear Cells from Patients with Myeloma.
S. Liu, H. Ishikawa, F.-J. Li, Z. Ma, K.-i. Otsuyama, H. Asaoku, S. Abroun, X. Zheng, N. Tsuyama, M. Obata, et al. (2005)
Cancer Res.
65, 2269-2276
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Peroxisome Proliferator-activated Receptor-{beta}/{delta} Inhibits Epidermal Cell Proliferation by Down-regulation of Kinase Activity.
D. J. Kim, I. A. Murray, A. M. Burns, F. J. Gonzalez, G. H. Perdew, and J. M. Peters (2005)
J. Biol. Chem.
280, 9519-9527
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Peroxisome Proliferator-Activated Receptor {delta} Suppresses 11{beta}-Hydroxysteroid Dehydrogenase Type 2 Gene Expression in Human Placental Trophoblast Cells.
L. Julan, H. Guan, J. P. van Beek, and K. Yang (2005)
Endocrinology
146, 1482-1490
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Peroxisome Proliferation-Activated Receptor (PPAR){gamma} Is Not Necessary for Synthetic PPAR{gamma} Agonist Inhibition of Inducible Nitric-Oxide Synthase and Nitric Oxide.
M. B. Crosby, J. L. Svenson, J. Zhang, C. J. Nicol, F. J. Gonzalez, and G. S. Gilkeson (2005)
J. Pharmacol. Exp. Ther.
312, 69-76
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PPAR- and LXR-dependent pathways controlling lipid metabolism and the development of atherosclerosis.
Modulation of Uncoupling Protein 1 and Peroxisome Proliferator-Activated Receptor {gamma} Expression in Adipose Tissue in Obese Insulin-Resistant Dogs.
V. Leray, C. Gayet, L. Martin, H. Dumon, B. Siliart, and P. Nguyen (2004)
J. Nutr.
134, 2154S-2157S
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Be Fit or Be Sick: Peroxisome Proliferator-Activated Receptors Are Down the Road.
B. Desvergne, L. Michalik, and W. Wahli (2004)
Mol. Endocrinol.
18, 1321-1332
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promotes lipid uptake and efflux in these atherogenic cells. In contrast, we found that the closely related receptor PPAR
controls the inflammatory status of the macrophage. Deletion of PPAR
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