Statins and foam cell formation: Impact on LDL oxidation and uptake of oxidized lipoproteins via scavenger receptors

Hofnagel, Oliver; Luechtenborg, Birgit; Weißen-Plenz, Gabriele; Robenek, Horst

doi:10.1016/j.bbalip.2007.06.003

Cited by 39 publications

(26 citation statements)

References 75 publications

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“…supported by the complication that uptake of modified lipoproteins by scavenger receptors is thought to be central to foam cell formation (56), which has previously been observed to occur over a relatively long time period (1-3 h) (55) and could confound our observation of binding and internalization of oxLDL. Studies of cells are also complicated because FA bind to the lipid bilayer, and most of the added FA may bind (partition) to the plasma membrane surrounding CD36 (Fig.…”

Section: Fatty Acid Cd36 Binding Increased Oxldl Uptakementioning

confidence: 71%

CD36 Binds Oxidized Low Density Lipoprotein (LDL) in a Mechanism Dependent upon Fatty Acid Binding

Jay

Chen

Paz

et al. 2015

Journal of Biological Chemistry

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Background: CD36 is expressed in many cell types and binds diverse ligands including oxidized LDL (oxLDL) and unesterified fatty acid (FA). Results: FA bind to CD36, which leads to oxLDL binding and uptake independent of CD36 disulfide bonds. Conclusion: Typical dietary FA enhance uptake of oxLDL. Significance: This study provides a possible mechanism for oxLDL binding CD36 that is dependent upon specific FA types.

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Section: Fatty Acid Cd36 Binding Increased Oxldl Uptakementioning

confidence: 71%

CD36 Binds Oxidized Low Density Lipoprotein (LDL) in a Mechanism Dependent upon Fatty Acid Binding

Jay

Chen

Paz

et al. 2015

Journal of Biological Chemistry

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“…As an inducing factor, MIF takes part in macrophage trapping around arterial intima and the forming of foam cells [34] , although the expression of MIF may be diminished in the macrophage-derived foam cells and macrophages in advanced atherosclerotic plaques [34] . Ox-LDL can inhibit macrophage random migration away from the artery through upregulating MIF, CD36 and scavenger receptor-A (SR-A) [33] , resulting in the accumulation of macrophages at the injury site in atherosclerotic lesions.…”

Section: Discussionmentioning

confidence: 99%

“…Ox-LDL can inhibit macrophage random migration away from the artery through upregulating MIF, CD36 and scavenger receptor-A (SR-A) [33] , resulting in the accumulation of macrophages at the injury site in atherosclerotic lesions. Macrophage recruitment that has been induced by MIF at least partially relies on enhanced expression of some other inflammatory mediators, such as ICAM-1, which inhibits macrophage migration directly [34,35] . Our research provides evidence that exendin-4 at 25 nmol/L and 50 nmol/L could relieve ox-LDL-induced inhibition of peritoneal macrophage migration, at least partially by regulating ox-LDL receptor CD36 and its downstream regulator MIF.…”

Section: Discussionmentioning

confidence: 99%

Exendin-4 ameliorates oxidized-LDL-induced inhibition of macrophage migration in vitro via the NF-κB pathway

Chen

Yin

et al. 2013

Acta Pharmacol Sin

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Aim: To investigate the effects of the glucagon-like peptide-1 (GLP-1) receptor agonist exendin-4 on oxidized low-density lipoprotein (ox-LDL)-induced inhibition of macrophage migration and the mechanisms underlying the effects of exendin-4. Methods: Primary peritoneal macrophages were extracted from the peritoneal cavity of mice treated with 3% thioglycollate (2 mL, ip). Migration of the macrophages was examined using a cell migration assay. Macrophage migration-related factors including leptin-like ox-LDL receptor (LOX-1), cyclooxygenase 2 (COX-2), tumor necrosis factor (TNF)-α, interleukin-1 (IL-1)β, matrix metalloproteinase-2 (MMP-2), intercellular adhesion molecule (ICAM)-1 and macrophage migration inhibitory factor (MIF) were measured using semiquantitative RT-PCR. Expression of MIF and ICAM-1 proteins was examined with ELISA. Gelatin zymography was used to evaluate the activity of MMP-9. Activation of the NF-κB pathway was determined by confocal laser scanning microscopy. Results: Treatment of the macrophages with ox-LDL (50 μg/mL) markedly suppressed the macrophage migration. Furthermore, ox-LDL treatment substantially increased the expression of the macrophage migration-related factors, the activity of MMP-9 and the translocation of the NF-κB p65 subunit. These effects of ox-LDL were significantly ameliorated by pretreatment with the specific NF-κB inhibitor ammonium pyrrolidine dithiocarbamate (100 μmol/L). These effects of ox-LDL were also significantly ameliorated by pretreatment with exendin-4 (25 and 50 nmol/L). Conclusion: Exendin-4 ameliorates the inhibition of ox-LDL on macrophage migration in vitro, via suppressing ox-LDL-induced expression of ICAM-1 and MIF, which is probably mediated by the NF-κB pathway.

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“…These molecules are expressed by endothelial and/or vascular smooth muscle cells upon proatherogenic stimuli such as oxidized LDL or oxidative free radicals [163,164]. After monocytes and T lymphocytes bind to the surface of the arterial wall, they migrate into the subendothelial space, where they differentiate and are transformed into macrophages and foam cells.…”

Section: Flavonoids Inflammation and Cancermentioning

confidence: 99%

Flavonoids as anti-inflammatory agents: implications in cancer and cardiovascular disease

et al. 2009

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Chronic inflammation is being shown to be increasingly involved in the onset and development of several pathological disturbances such as arteriosclerosis, obesity, diabetes, neurodegenerative diseases and even cancer. Treatment for chronic inflammatory disorders has not been solved, and there is an urgent need to find new and safe anti-inflammatory compounds. Flavonoids belong to a group of natural substances occurring normally in the diet that exhibit a variety of beneficial effects on health. The anti-inflammatory properties of flavonoids have been studied recently, in order to establish and characterize their potential utility as therapeutic agents in the treatment of inflammatory diseases. Several mechanisms of action have been proposed to explain in vivo flavonoid anti-inflammatory actions, such as antioxidant activity, inhibition of eicosanoid generating enzymes or the modulation of the production of proinflammatory molecules. Recent studies have also shown that some flavonoids are modulators of proinflammatory gene expression, thus leading to the attenuation of the inflammatory response. However, much work remains to be done in order to achieve definitive conclusions about their potential usefulness. This review summarizes the known mechanisms involved in the anti-inflammatory activity of flavonoids and the implications of these effects on the protection against cancer and cardiovascular disease.

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Statins and foam cell formation: Impact on LDL oxidation and uptake of oxidized lipoproteins via scavenger receptors

Cited by 39 publications

References 75 publications

CD36 Binds Oxidized Low Density Lipoprotein (LDL) in a Mechanism Dependent upon Fatty Acid Binding

CD36 Binds Oxidized Low Density Lipoprotein (LDL) in a Mechanism Dependent upon Fatty Acid Binding

Exendin-4 ameliorates oxidized-LDL-induced inhibition of macrophage migration in vitro via the NF-κB pathway

Flavonoids as anti-inflammatory agents: implications in cancer and cardiovascular disease

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