High-Density Lipoproteins Suppress Chemokines and Chemokine Receptors In Vitro and In Vivo
| Autor: | Douglas T. Beattie, Shirley Nakhla, Emiel P. C. van der Vorst, Kerry-Anne Rye, Philip J. Barter, Alison K. Heather, Maria L. Castro, Christina A. Bursill |
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| Rok vydání: | 2010 |
| Předmět: |
CCR2
Chemokine medicine.medical_specialty Receptors CCR2 Down-Regulation IκB kinase CCL2 Monocytes CCL5 Receptors Interleukin-8A Mice Chemokine receptor Apolipoproteins E NF-KappaB Inhibitor alpha Internal medicine medicine Animals Humans RNA Messenger Sulfones Phosphorylation Receptor Chemokine CCL5 Cells Cultured Chemokine CCL2 Mice Knockout Apolipoprotein A-I biology Chemokine CX3CL1 Transcription Factor RelA Endothelial Cells Isoxazoles Atherosclerosis Mice Inbred C57BL PPAR gamma Chemotaxis Leukocyte Disease Models Animal IκBα Endocrinology Injections Intravenous biology.protein I-kappa B Proteins Receptors Chemokine Chemokines Lipoproteins HDL Cardiology and Cardiovascular Medicine |
| Zdroj: | Arteriosclerosis, Thrombosis, and Vascular Biology. 30:1773-1778 |
| ISSN: | 1524-4636 1079-5642 |
| Popis: | Objective— To investigate whether high-density lipoproteins (HDLs) suppress chemokine (CCL2, CCL5, and CX 3 CL1) and chemokine receptor (CCR2 and CX 3 CR1) expression, a mechanism for the atheroprotective properties of HDLs. Methods and Results— Apolipoprotein (apo) E −/− mice were fed a high-fat diet for 12 weeks. Before being euthanized, the mice received 5 consecutive daily injections of lipid-free apoA-I, 40 mg/kg, or saline (control). The injection of apoA-I reduced CCR2 and CX 3 CR1 expression in plaques compared with controls ( P 3 CL1 levels were also reduced ( P 3 CR1 expression and inhibited their migration toward CCL2 and CX 3 CL1 ( P 3 CL1 expression in monocytes and human coronary artery endothelial cells. The stimulation of CX 3 CR1 with peroxisome proliferator–activated receptor γ agonist CAY10410 was suppressed by preincubation with rHDL but did not affect the peroxisome proliferator–activated receptor γ antagonist (GW9664)–mediated increase in CCR2. In monocytes and human coronary artery endothelial cells, rHDL reduced the expression of the nuclear p65 subunit, IκB kinase activity, and the phosphorylation of IκBα ( P Conclusion— Lipid-free apoA-I and rHDL reduce the expression of chemokines and chemokine receptors in vivo and in vitro via modulation of nuclear factor κB and peroxisome proliferator–activated receptor γ. |
| Databáze: | OpenAIRE |
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