Effects of activation on lipid and lipoprotein metabolism in murine macrophages.

Kraemer, Fredric B.; Tavangar, Kamran; Gandjei, R K.; Kirlew, Konrad; Behr, Stephen R.

doi:10.1161/01.atv.10.1.8

Cited by 24 publications

(10 citation statements)

References 53 publications

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“…Only a few The mechanism underlying these differences is unclear, but a growing body of evidence suggests (25). Similarly, several investigators found that IFN-'y inhibits AcLDL degradation in activated murine macrophages (26,44 …”

Section: Resultsmentioning

confidence: 99%

Regulation of smooth muscle cell scavenger receptor expression in vivo by atherogenic diets and in vitro by cytokines.

Freeman²,

Libby³

1995

J. Clin. Invest.

169

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Section: Resultsmentioning

confidence: 99%

Regulation of smooth muscle cell scavenger receptor expression in vivo by atherogenic diets and in vitro by cytokines.

Freeman²,

Libby³

1995

J. Clin. Invest.

169

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“…They found, however, that poly:I:C, which is an inducer of a-and ,B-interferons and an activator of macrophages, inhibited AcLDL degradation (35). Finally, Kraemer et al (36) found a reduction of 60% in AcLDL binding by the activated murine macrophages but no effect of activation on the affinity of AcLDL for ScR.…”

Section: Discussionmentioning

confidence: 96%

Interferon-gamma inhibits scavenger receptor expression and foam cell formation in human monocyte-derived macrophages.

1992

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The scavenger receptor (ScR) mediates uptake of chemically modified low density lipoprotein (LDL) by human monocytederived macrophages. It is not down-regulated by high intracellular cholesterol levels, and exposure of macrophages to acetylated or oxidized LDL therefore leads to foam cell development. The hypothesis that this represents an important mechanism for intracellular cholesterol accumulation in atherosclerosis is supported by the finding of ScR expression in foam cells of atherosclerotic plaques. T lymphocytes are also present in such plaques and it is known that T cell products regulate macrophage activation. We have therefore studied the effect of interferon-'y (IFN'y), a lymphokine secreted by activated T lymphocytes, on the expression of ScR in human monocytederived macrophages. Binding and uptake of acetylated LDL were significantly reduced in macrophages exposed to recombinant IFNy or IFN-y-containing lymphocyte-conditioned media. Competition experiments showed that the IFNy-regulated binding and uptake of acetylated LDL was mediated via ScR. IFN

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“…26 This may be related to the different stimuli as well as to the fact that macrophage stimulation in that study 26 was obtained by injection of the activators into the mice, whereas the LPS in our study was incubated directly with the cells, and thus, different cellular metabolic properties may have been affected. Increased LDL uptake by activated macrophages could be related (from the Scatchard plot) to increments in both the number of LDL binding sites and the affinity of the lipoprotein to its receptor (increased "apparent B ,^" and reduced "apparent K m ").…”

mentioning

confidence: 83%

Increased susceptibility to activation and increased uptake of low density lipoprotein by cholesterol-loaded macrophages.

Oiknine

Aviram

1992

Arterioscler Thromb

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Inflammation is associated with macrophage activation, and this process has been shown to occur during atherogenesis. Macrophages (J774A.1) that were activated with either lipopolysaccharide (LPS), zymosan, or phorbol ester demonstrated a 30-35% increased uptake and degradation of low density lipoprotein (LDL) in comparison with nonactivated cells. This phenomenon was also shown for LDL cellular binding, and it resulted in macrophage cholesterol accumulation, as evidenced by cholesterol mass determination and flow cell cytometric analysis. Enhanced uptake of LDL was also obtained with two other types of macrophages: mouse peritoneal macrophages and human monocyte-derived macrophages. In LPSstimulated macrophages, high density lipoprotein-mediated cholesterol efflux was not different from that shown in nonstimulated cells. Cellular cholesterol synthesis, however, was increased by 25% in the activated macrophages. Macrophage activation, measured as cellular procoagulant activity, was higher in cholesterol-loaded than in nonloaded cells. On stimulation of cholesterol-loaded macrophages, cellular uptake and degradation of LDL were increased by 3.3-fold in comparison with nonactivated cholesterolloaded cells. Human monocyte-derived macrophages from hypercholesterolemic patients were found to contain 52% more cholesterol mass than macrophages derived from normal healthy donors. These cells demonstrated increased activation (twofold) in response to LPS stimulation and also showed 25% enhanced cellular degradation of LDL. We conclude that activation of macrophages during atherogenesis can lead to foam cell formation, and this mechanism is probably operative in hypercholesterolemic

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Effects of activation on lipid and lipoprotein metabolism in murine macrophages.

Cited by 24 publications

References 53 publications

Regulation of smooth muscle cell scavenger receptor expression in vivo by atherogenic diets and in vitro by cytokines.

Regulation of smooth muscle cell scavenger receptor expression in vivo by atherogenic diets and in vitro by cytokines.

Interferon-gamma inhibits scavenger receptor expression and foam cell formation in human monocyte-derived macrophages.

Increased susceptibility to activation and increased uptake of low density lipoprotein by cholesterol-loaded macrophages.

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