Inhibition of macrophage inflammatory cytokine secretion by chylomicron remnants is dependent on their uptake by the low density lipoprotein receptor

Graham, V.; Maggio, Paola; Armengol, Sandra; Wheeler‐Jones, Caroline P.D.; Botham, Kathleen M.

doi:10.1016/j.bbalip.2010.11.008

Cited by 7 publications

(11 citation statements)

References 44 publications

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“…272,273) To investigate the mechanisms of CM remnant-induced atherosclerosis, I have prepared FC-containing emulsion particles as a model for CM remnants. ApoE promotes the uptake of lipid emulsions by J774 macrophages.…”

Section: Remnantsmentioning

confidence: 99%

Metabolism and Modification of Apolipoprotein B-Containing Lipoproteins Involved in Dyslipidemia and Atherosclerosis

Morita

2016

Biological & Pharmaceutical Bulletin

132

113

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Increased levels of apolipoprotein B (apoB)-containing lipoproteins, such as low density lipoproteins (LDL) and chylomicron remnants, are associated with the development of atherosclerosis. Chylomicrons containing apoB-48 are secreted from the intestine during the postprandial state, whereas very low density lipoproteins (VLDL) containing apoB-100 are constitutively formed in the liver. Chylomicron remnants and VLDL remnants are produced by the lipoprotein lipase-mediated lipolysis of triglycerides, which is activated by apolipoprotein C-II bound on the particle surfaces. The hepatic uptake of these remnants is facilitated by apolipoprotein E (apoE), but is inhibited by apolipoproteins C-I, C-II and C-III. In the plasma, VLDL remnants are further converted into LDL by the hydrolysis of triglycerides. ApoB-100 is responsible for the hepatic uptake of LDL. LDL receptor, LDL receptor-related protein and heparan sulfate proteoglycans are involved in the hepatic clearance of lipoproteins containing apoB-100 and/or apoE. The subendothelial retention and modification of apoB-containing lipoproteins are crucial events in the initiation of atherosclerosis. In the subendothelium, the uptake of modified lipoproteins by macrophages leads to the formation of foam cells storing excess amounts of cholesteryl esters and subsequently to apoptosis. This review describes the current knowledge about the metabolism and modification of apoB-containing lipoproteins involved in dyslipidemia and atherogenesis. In particular, I focus on the effects of apolipoproteins, lipid composition and particle size on lipoprotein metabolism and on the roles of cholesterol, sphingomyelinase and apoB denaturation in macrophage foam cell formation and apoptosis. A detailed understanding of these mechanisms will help to develop new therapeutic strategies.

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Section: Remnantsmentioning

confidence: 99%

Metabolism and Modification of Apolipoprotein B-Containing Lipoproteins Involved in Dyslipidemia and Atherosclerosis

Morita

2016

Biological & Pharmaceutical Bulletin

132

113

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“…We have previously reported that denatured apoB induces macrophage apoptosis by disturbance of the plasma membrane [26]. It has been shown that chylomicron remnant-like particles downregulate the pro-inflammatory chemokine and cytokine secretion by monocytes and macrophages [27,28]. More recently, it has been reported that ezetimibe and simvastatin increase the removal of chylomicron-like emulsions from plasma in coronary heart disease subjects [29].…”

Section: Contents Lists Available At Sciencedirectmentioning

confidence: 96%

Chylomicron remnant model emulsions induce intracellular cholesterol accumulation and cell death due to lysosomal destabilization

Wakita

Morita

Okamoto

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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“…Furthermore, we have also found that these lipoproteins influence the secretion of proinflammatory chemokines and cytokines by HMDM and THP-1 macrophages via regulation at the transcriptional level [21, 22]. …”

Section: Introductionmentioning

confidence: 99%

“…Unlike LDL, CMRs are able to induce their effects on macrophage foam cell formation and on proinflammatory cytokine secretion without prior oxidation [16–22]. However, our earlier work has demonstrated that, in striking contrast to the effects of LDL oxidation, the oxidative state of CMRs is inversely related to their ability to induce foam cell formation.…”

Section: Introductionmentioning

confidence: 99%

“…Thus, when CMRs are protected from oxidation by incorporation of antioxidants into the particles, lipid accumulation in macrophages is increased [17, 23], while oxidation of CMRs inhibits their ability to induce foam cell formation [18, 24]. Our studies have also shown that the oxidative state of CMRs plays an important role in their effects on proinflammatory cytokine secretion by macrophages [22]. …”

Section: Introductionmentioning

confidence: 99%

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The Oxidative State of Chylomicron Remnants Influences Their Modulation of Human Monocyte Activation

Lopez

Botham

2012

International Journal of Vascular Medicine

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Chylomicron remnants (CMRs) contribute directly to human monocyte activation in vitro, by increasing reactive oxygen species (ROS) production and cell migration. In this study, the effects of the oxidative state of CMR on the degree of monocyte activation was investigated. CMR-like particles (CRLPs) were prepared in three different oxidative states, normal (CRLPs), protected from oxidation by incorporation of the antioxidant, probucol (pCRLPs), or oxidised with CuSO4 (oxCRLPs). Lipid accumulation and ROS production were significantly increased in primary human monocytes incubated with CRLPs, whilst secretion on monocyte chemoattractant protein-1 was reduced, but oxCRLPs had no additional effect. In contrast, pCRLPs were taken up by monocytes to a lesser extent and had no significant effect on ROS or MCP-1 secretion. These studies suggest that the oxidative state of CMRs modulates their stimulation of the activation of peripheral blood human monocytes and that dietary antioxidants may provide some protection against these atherogenic effects.

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Inhibition of macrophage inflammatory cytokine secretion by chylomicron remnants is dependent on their uptake by the low density lipoprotein receptor

Cited by 7 publications

References 44 publications

Metabolism and Modification of Apolipoprotein B-Containing Lipoproteins Involved in Dyslipidemia and Atherosclerosis

Metabolism and Modification of Apolipoprotein B-Containing Lipoproteins Involved in Dyslipidemia and Atherosclerosis

Chylomicron remnant model emulsions induce intracellular cholesterol accumulation and cell death due to lysosomal destabilization

The Oxidative State of Chylomicron Remnants Influences Their Modulation of Human Monocyte Activation

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