Impact of monocyte colony-stimulating factor upon β-very low density lipoprotein (β-VLDL) cholesterol metabolism in tetradecanoyl phorbol acetate-derived THP-1 cells

Ishii, Itsuko; Yanagimachi, Mamoru; Shirai, Kohji; Saitō, Yasushi; Hirose, Sachiko

doi:10.1016/0005-2760(94)90201-1

Cited by 12 publications

(4 citation statements)

References 18 publications

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“…However, 4°C binding studies using both 125 I-LDL and 125 I-␤-VLDL indicated that M-CSF did not enhance lipoprotein metabolism via increasing cell surface lipoprotein receptor (LDL receptor) expression. In contrast to our findings, prolonged exposure (4 days) of a human monocyte-derived macrophage cell line (tetradecanoyl phorbol acetate-treated THP-1cells) to M-CSF had no affect on ␤-VLDLinduced cholesterol ester deposition (31). Possible explanations to account for this discrepancy may include desensitization of an M-CSF signaling pathway in response to prolonged incubation with the cytokine, or changes in an M-CSF signaling pathway following prolonged exposure to the phorbol ester used to differentiate THP-1 monocytes.…”

Section: M-csf Enhances ␤-Vldl Metabolism Via G I/o Protein Activation-contrasting

confidence: 56%

Macrophage Colony-stimulating Factor Rapidly Enhances β-Migrating Very Low Density Lipoprotein Metabolism in Macrophages through Activation of a Gi/o Protein Signaling Pathway

Whitman¹,

Daugherty²,

Post³

2000

Journal of Biological Chemistry

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Section: M-csf Enhances ␤-Vldl Metabolism Via G I/o Protein Activation-contrasting

confidence: 56%

Macrophage Colony-stimulating Factor Rapidly Enhances β-Migrating Very Low Density Lipoprotein Metabolism in Macrophages through Activation of a Gi/o Protein Signaling Pathway

Whitman¹,

Daugherty²,

Post³

2000

Journal of Biological Chemistry

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“…The fact that cholesterol accumulation occurred in our study but not in these previous studies can be attributed in part to PMA activation of the macrophages here which caused a substantial increase in LDL uptake by the macrophages. Also, PMA activation of macrophages has been reported to increase ACAT activity, which could increase cholesterol esterification (43). Previously, it was shown that reductive methylation of LDL decreases the saturable nonspecific low affinity binding uptake of LDL observed at high LDL concentrations (44).…”

Section: Table IV Evaluation Of Ldl Receptor Function In Cholesterol mentioning

confidence: 99%

Macrophage Foam Cell Formation with Native Low Density Lipoprotein

Kruth

Huang

Ishii

et al. 2002

Journal of Biological Chemistry

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137

118

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This investigation has elucidated a mechanism for development of macrophage foam cells when macrophages are incubated with native low density lipoprotein (LDL). LDL is believed to be the main source of cholesterol that accumulates in monocyte-derived macrophages within atherosclerotic plaques, but native LDL has not previously been shown to cause substantial cholesterol accumulation when incubated with macrophages. We have found that activation of human monocyte-derived macrophages with phorbol 12-myristate 13-acetate ( Engorgement of macrophages with cholesterol is the defining pathological characteristic of atherosclerotic plaques, the cause of most heart attacks and strokes. Cholesterol accumulation in macrophages not only contributes to cholesterol retention within the vessel wall, but also alters macrophage biology. Cholesterol-loaded macrophages secrete plaque-disrupting matrix metalloproteinases, and produce tissue factor that promotes thrombosis when plaques rupture (1-3). Thus, how macrophages accumulate cholesterol and become foam cells has been the subject of intense investigation.Low density lipoprotein (LDL), 1 the main carrier of plasma cholesterol, enters the vessel wall and then by some mechanism enters macrophages. Previously, native LDL could not be shown to cause foam cell formation because the cellular receptor that binds LDL is poorly expressed on differentiated macrophages and down-regulates during cholesterol uptake, limiting total cholesterol accumulation (4 -7). Moreover, the LDL receptor is not expressed in human atherosclerotic plaques (8). Thus, most previous studies of macrophage foam cell formation have focused on modifying LDL in some way that increases its binding to macrophages. Increased macrophage binding of LDL has been achieved with chemical modifications to the apoB component of the LDL, aggregation of LDL induced by either vortexing or treatment of LDL with lipases, and complexing of LDL with other molecules, for example, glycosaminoglycans or antibodies, which bind macrophages and promote LDL uptake by piggyback endocytosis (9). Macrophages take up modified LDL by receptormediated endocytosis in pinocytotic vesicles, phagocytic vacuoles, or patocytic surface-connected compartments (9).One popular hypothesis of foam cell formation involves LDL oxidation. LDL oxidation promotes macrophage LDL uptake that is mediated by various macrophage scavenger receptors (10). Although oxidation of LDL has important biological effects that could influence atherosclerotic plaque development (11), oxidation of LDL does not readily explain foam cell formation. Incubation of human monocyte-derived macrophages with oxidized LDL, even strongly oxidized with artificial chemical systems, produces little macrophage cholesterol accumulation (12, 13). Also, oxidized LDL is poorly metabolized within lysosomes of macrophages because of partial inactivation by oxidized LDL of the lysosomal enzymes that degrade LDL (14 -16). This limits the capacity of oxidized LDL to induce acyl-CoA:cholesterol acyltra...

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“…They are known to be induced for macrophage-like functions, including expression of the genes encoding the scavenger receptor and the MCSF receptor in certain conditions such as stimulation by PDGF BB (Inaba et al, 1992a(Inaba et al, , 1992b. MCSF is known to enhance the activity of macrophage (Nakoinz and Ralph, 1988;Hume et al, 1988;Ishibashi et al, 1990;Shimano et al, 1990;Mori et al, 1991;Inaba et al, 1993;Ishii et al, 1994), and PMA is used for inducing differentiation of macrophage cell line cells such as THP-1 cells with respect to a number of macrophage-like functions, including expression of the scavenger receptor (Hara et al, 1987;Takata et al, 1989) and secretion of lipoprotein lipase and apolipoprotein E Menju et al, 1989).…”

Section: Table IVmentioning

confidence: 99%

Independent Regulation of Cholesterol Incorporation into Free Apolipoprotein-mediated Cellular Lipid Efflux in Rat Vascular Smooth Muscle Cells

Yokoyama

1995

Journal of Biological Chemistry

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Cholesterol was poorly available to free apolipoprotein (apo)A-I-mediated cellular lipid efflux from cholesterol-loaded rat vascular smooth muscle cells generating cholesterol-poorer pre-␤-HDL particles than those generated from macrophages by the same reaction (Li, Q., Komaba, A., and Yokoyama, S. (1993) Biochemistry 32, 4597-4603). The factors known to induce transformation of the smooth muscle cells into a macrophage-like stage were used in order to modulate this reaction, such as human platelet-derived growth factor, macrophage colony-stimulating factor, and phorbol 12-myristate-13-acetate (PMA). When the cells were stimulated by PMA following the pretreatment with platelet-derived growth factor plus macrophage colony-stimulating factor, cholesterol efflux mediated by free apoA-I increased 3-fold without changing phospholipid efflux, resulting in generation of pre-␤-HDL particles more rich in cholesterol. This treatment had only a little or no effect on apparent cellular cholesterol efflux to HDL or lipid microemulsion, respectively. Overall cellular free cholesterol pool size was unaffected by the treatment, and probing by extracellular cholesterol oxidase did not detect gross change in the cellular surface cholesterol. This specific enrichment of cholesterol in the apoA-Imediated cellular lipid efflux was reversed by protein kinase C inhibitors. Measurement of intracellular cholesterol esterification suggested that PMA induced translocation of intracellular cholesterol to a specific pool for apoA-I-mediated efflux, and a protein kinase C inhibitor reversed this effect.

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Impact of monocyte colony-stimulating factor upon β-very low density lipoprotein (β-VLDL) cholesterol metabolism in tetradecanoyl phorbol acetate-derived THP-1 cells

Cited by 12 publications

References 18 publications

Macrophage Colony-stimulating Factor Rapidly Enhances β-Migrating Very Low Density Lipoprotein Metabolism in Macrophages through Activation of a Gi/o Protein Signaling Pathway

Macrophage Colony-stimulating Factor Rapidly Enhances β-Migrating Very Low Density Lipoprotein Metabolism in Macrophages through Activation of a Gi/o Protein Signaling Pathway

Macrophage Foam Cell Formation with Native Low Density Lipoprotein

Independent Regulation of Cholesterol Incorporation into Free Apolipoprotein-mediated Cellular Lipid Efflux in Rat Vascular Smooth Muscle Cells

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