Effect of glucose-mediated LDL oxidation on the P388D1 macrophage-like cell line

Millican, Stephanie A.; Bagga, M.; Eddy, Rachel L.; Mitchinson, M. J.; Hunt, James V.

doi:10.1016/s0021-9150(96)06004-2

Cited by 4 publications

(1 citation statement)

References 54 publications

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“…The murine P388D1 macrophage-like cell line, a well-studied model for investigating human atherogenesis ( 32,33 ), was obtained from the American Type Culture Collection (Rockville, MD). Cultures were maintained in exponential growth (between 2 × 10 5 cells/ml and 1.5 × 10 6 cells/ml) at 37°C, 5% CO 2 in T-25 cm 2 tissue culture fl asks (Falcon, M19, Milan, Italy) containing RPMI 1640 medium supplemented with 10% bovine calf serum (BCS) (Bioquote Ltd., York, UK), streptomycin (100 g/ml), L -glutamine (2 mM), and penicillin (100 U/ml).…”

Section: Cellsmentioning

confidence: 99%

Role of HDL in cholesteryl ester metabolism of lipopolysaccharide-activated P388D1 macrophages

Uda

Spolitu

Angius

et al. 2013

Journal of Lipid Research

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This article is available online at http://www.jlr.org hallmark of atherosclerosis. Similar changes are present in chronic metabolic diseases (hypercholesterolemia, insulin resistance, diabetes, etc.) ( 4 ), and have been described in other disorders such as cancer ( 5-9 ) and infections ( 10 ). Probably, accumulation of CEs serves as a reservoir of cholesterol for an enhanced membrane biogenesis during sustained proliferation.During acute infections the body undergoes several metabolic changes ( 11,12 ), among which plasma lipid alterations are prominent and related to a shift in energetic requirements (increased triglycerides and fatty acids) ( 13,14 ) or to structural modifi cation of LDLs ( 15 ) and HDLs ( 16,17 ). The infection-related decrease in C-HDLs observed in all species is ascribed to a reduction of proteins involved in reverse cholesterol transport ( 18,19 ), supposedly induced by infl ammatory molecules secreted from immune cells activated by the microbial stimulus ( 16 ). Thus, during infection, an ineffi cient removal of cholesterol from the arteries may contribute toward eliciting a lipid overload of macrophages and transformation of the former into foam cells ( 19 ). For this reason, infections have been considered as a serious risk factor for the development or worsening of atherosclerosis (20)(21)(22). Epidemiological fi ndings support this correlation, with acute vascular accidents (myocardial infarction, ictus, etc.) being described during acute and chronic infections. Carotid plaques have been observed in patients with periodontal diseases ( 23, 24 ) and other chronic infections ( 25,26 ).

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Section: Cellsmentioning

confidence: 99%

Role of HDL in cholesteryl ester metabolism of lipopolysaccharide-activated P388D1 macrophages

Uda

Spolitu

Angius

et al. 2013

Journal of Lipid Research

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The Roles of Protein Glycation, Glycoxidation, and Advanced Glycation End-Product Formation in Diabetes-Induced Atherosclerosis

Rashid

Brown

Reyk

et al. 2006

Biochemistry of Atherosclerosis

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Glycoxidation and lipid peroxidation of low-density lipoprotein can synergistically enhance atherogenesis

Sakata

Uesugi

Takebayashi

et al. 2001

Cardiovascular Research

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Objective: The purpose of this study was to clarify the role of glycoxidation and lipid peroxidation of low-density lipoprotein (LDL) in e atherogenesis. Methods and results: We examined the formation of N -(carboxymethyl) lysine (CML), a glycoxidation product, and malondialdehyde (MDA), a lipid peroxidation product, in vitro and their co-localization in human atherosclerotic lesions. Immunochemical analysis revealed that CML was formed in a time-dependent manner by human LDL incubated with copper ions and glucose, i.e. an in vitro model of glycoxidation of LDL. When LDL was exposed to copper ions alone, a small amount of CML was formed, however this was significantly less in oxidized LDL than glycoxidative LDL. In contrast, MDA formation was observed in both oxidation and glycoxidation of LDL, but not in glycation of LDL. Hexitol-lysine (HL), an Amadori product, was formed by both glycation and glycoxidation of LDL, but not by oxidation of LDL. Immunohistochemical analysis showed that CML and MDA accumulated mainly in macrophage / foam cells, while pyrraline, a non-oxidative product of glycation, and apolipoprotein B were localized in the extracellular matrix in atherosclerotic lesions. Atheromas were positive for CML and MDA, but negative for pyrraline. Macrophage / foam cells in atherosclerotic lesions exhibited co-localization of macrophage scavenger receptor-A with CML and MDA, but not with pyrraline. Conclusion: Our results suggest that glycoxidation and lipid peroxidation of LDL synergistically promote the development of atherosclerotic lesions through interaction with macrophage scavenger receptor-A.

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Effect of glucose-mediated LDL oxidation on the P388D1 macrophage-like cell line

Cited by 4 publications

References 54 publications

Role of HDL in cholesteryl ester metabolism of lipopolysaccharide-activated P388D1 macrophages

Role of HDL in cholesteryl ester metabolism of lipopolysaccharide-activated P388D1 macrophages

The Roles of Protein Glycation, Glycoxidation, and Advanced Glycation End-Product Formation in Diabetes-Induced Atherosclerosis

Glycoxidation and lipid peroxidation of low-density lipoprotein can synergistically enhance atherogenesis

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