1996

DOI: 10.1016/0024-3205(95)02351-8

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Mature human atherosclerotic plaque contains peroxidized phosphatidylcholine as a major lipid peroxide

Joseph J. Piotrowski

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,

Syed Mahmood Shah

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,

Robert R. Alexander

³

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Cited by 33 publications

(31 citation statements)

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“…Indeed, although MDA-LDL is only 1 of many epitopes of OxLDL, it is clearly ubiquitous in atherosclerotic lesions. 3,5,6,13,15,16,38,39 The correlations with lesion size were also much better for MDA-LDL than for Cu-OxLDL autoantibodies. Besides MDA-lysine epitopes, copper-induced oxidation of LDL also generates many other epitopes, such as oxidized phospholipids.…”

Section: Discussionmentioning

confidence: 84%

“…1 Human atherosclerotic lesions have been shown to contain abundant quantities of oxidized lipoproteins within foam cells and in the extracellular space. [2][3][4][5][6] In patients with myocardial infarction, atherosclerotic lesions undergoing plaque rupture, erosion, and thrombosis often contain large lipid pools with significant amounts of extracellular oxidized lipids and oxidized LDL (Ox-LDL). 7,8 Indeed, recent evidence suggests that plasma levels of malondialdehyde (MDA)-LDL, an epitope of OxLDL derived from lipid peroxidation, is elevated in patients with coronary artery disease and is a strong predictor of acute coronary syndromes.…”

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confidence: 99%

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Circulating Autoantibodies to Oxidized LDL Correlate With Arterial Accumulation and Depletion of Oxidized LDL in LDL Receptor–Deficient Mice

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2001

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Abstract-Autoantibodies to oxidized low density lipoprotein (OxLDL) are elevated in some human populations with increased risk of atherosclerosis. To determine whether autoantibody levels to epitopes of OxLDL reflect the extent of aortic atherosclerosis and the content of OxLDL, we measured IgG and IgM autoantibody titers to malondialdehyde (MDA)-LDL and copper-oxidized LDL (Cu-OxLDL) in 43 LDL receptor-deficient mice consuming atherogenic and regression diets. Antibody titers were correlated to percent atherosclerotic surface area, aortic weight, and aortic OxLDL content, measured as the in vivo uptake of 125 I-MDA2, a monoclonal antibody to MDA-LDL. All mice were fed an atherogenic diet for 6 months, and 1 group was euthanized. The other 3 groups were fed an atherogenic diet (fat/CHOL group), normal mouse chow (chow group), or mouse chow supplemented with vitamins E and C (chowϩVIT group) for an additional 6 months. After dietary intervention, compared with their own baseline, autoantibody titers to MDA-LDL and Cu-OxLDL increased significantly in the fat/CHOL group, whereas they did not change or decreased significantly in the chow and chowϩVIT groups. Aortic weight and surface area showed significant progression in the fat/CHOL group, mild progression in the chow group, and no progression in the chowϩVIT group (PϽ0.001), whereas OxLDL content actually decreased in the latter 2 groups (PϽ0.001). Significant correlations were seen with MDA-LDL autoantibody titers and OxLDL content (IgM, Rϭ0.64 and Pϭ0.0009; IgG, Rϭ0.52 and Pϭ0.009), as well as with percent surface area and aortic weight. These data support the hypothesis that autoantibody titers to OxLDL reflect changes in OxLDL content in atherosclerotic lesions of LDL receptor-deficient mice. Whether autoantibody titers to OxLDL will provide similar valuable insights into the extent of human atherosclerosis, particularly anatomic measurements of plaque burden and OxLDL content, remains to be determined.

“…Indeed, although MDA-LDL is only 1 of many epitopes of OxLDL, it is clearly ubiquitous in atherosclerotic lesions. 3,5,6,13,15,16,38,39 The correlations with lesion size were also much better for MDA-LDL than for Cu-OxLDL autoantibodies. Besides MDA-lysine epitopes, copper-induced oxidation of LDL also generates many other epitopes, such as oxidized phospholipids.…”

Section: Discussionmentioning

confidence: 84%

“…1 Human atherosclerotic lesions have been shown to contain abundant quantities of oxidized lipoproteins within foam cells and in the extracellular space. [2][3][4][5][6] In patients with myocardial infarction, atherosclerotic lesions undergoing plaque rupture, erosion, and thrombosis often contain large lipid pools with significant amounts of extracellular oxidized lipids and oxidized LDL (Ox-LDL). 7,8 Indeed, recent evidence suggests that plasma levels of malondialdehyde (MDA)-LDL, an epitope of OxLDL derived from lipid peroxidation, is elevated in patients with coronary artery disease and is a strong predictor of acute coronary syndromes.…”

mentioning

confidence: 99%

Circulating Autoantibodies to Oxidized LDL Correlate With Arterial Accumulation and Depletion of Oxidized LDL in LDL Receptor–Deficient Mice

¹

,

²

,

³

2001

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Abstract-Autoantibodies to oxidized low density lipoprotein (OxLDL) are elevated in some human populations with increased risk of atherosclerosis. To determine whether autoantibody levels to epitopes of OxLDL reflect the extent of aortic atherosclerosis and the content of OxLDL, we measured IgG and IgM autoantibody titers to malondialdehyde (MDA)-LDL and copper-oxidized LDL (Cu-OxLDL) in 43 LDL receptor-deficient mice consuming atherogenic and regression diets. Antibody titers were correlated to percent atherosclerotic surface area, aortic weight, and aortic OxLDL content, measured as the in vivo uptake of 125 I-MDA2, a monoclonal antibody to MDA-LDL. All mice were fed an atherogenic diet for 6 months, and 1 group was euthanized. The other 3 groups were fed an atherogenic diet (fat/CHOL group), normal mouse chow (chow group), or mouse chow supplemented with vitamins E and C (chowϩVIT group) for an additional 6 months. After dietary intervention, compared with their own baseline, autoantibody titers to MDA-LDL and Cu-OxLDL increased significantly in the fat/CHOL group, whereas they did not change or decreased significantly in the chow and chowϩVIT groups. Aortic weight and surface area showed significant progression in the fat/CHOL group, mild progression in the chow group, and no progression in the chowϩVIT group (PϽ0.001), whereas OxLDL content actually decreased in the latter 2 groups (PϽ0.001). Significant correlations were seen with MDA-LDL autoantibody titers and OxLDL content (IgM, Rϭ0.64 and Pϭ0.0009; IgG, Rϭ0.52 and Pϭ0.009), as well as with percent surface area and aortic weight. These data support the hypothesis that autoantibody titers to OxLDL reflect changes in OxLDL content in atherosclerotic lesions of LDL receptor-deficient mice. Whether autoantibody titers to OxLDL will provide similar valuable insights into the extent of human atherosclerosis, particularly anatomic measurements of plaque burden and OxLDL content, remains to be determined.

“…Among oxidatively modified lipids, phosphatidylcholine hydroperoxide (PCOOH), a primary oxidation product of phosphatidylcholine (PC), was observed to be accumulated in arterial walls and blood plasma in atherosclerotic rabbits (5). PCOOH was also identified in human atherosclerotic lesions (6,7). Furthermore, PCOOH accumulation in plasma has been shown in human subjects with pathological conditions such as hyperlipidemia (8,9), diabetes (10), uremia (9), and alcoholism (11).…”

mentioning

confidence: 95%

Phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to intracellular adhesion molecule-1

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et al. 2009

Journal of Lipid Research

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The accumulation of phosphatidylcholine hydroperoxide (PCOOH), a primary oxidation product of phosphatidylcholine (PC), in blood plasma and tissues has been observed in various pathological conditions, including atherosclerosis. However, the biological roles of PCOOH in these conditions remain unknown. To estimate the atherogenicity of PCOOH, we evaluated the effect of PCOOH on THP-1 monocytic cell adherence to immobilized vascular endothelial cell adhesion molecules. THP-1 cell adhesion to intracellular adhesion molecule-1 (ICAM-1) was dosedependently increased by addition of PCOOH. Phosphatidylcholine hydroxide (a hydroxyl analog of PCOOH) also induced THP-1 cell adhesion to ICAM-1, whereas nonoxidized PC, sn-2 truncated PCs, and other hydroperoxide compounds did not affect the adhesion. In the PCOOH-treated cells, obvious protruding F-actin-rich membrane structures were formed, and lymphocyte function-associated antigen-1 (LFA-1) was localized to the protruding structures. Cytochalasin D, an actin polymerization inhibitor, suppressed the PCOOH-induced cell adhesion to ICAM-1 and the membrane protrusions. These results indicate that PCOOH evokes LFA-1-mediated cell adhesion to ICAM-1 via actin cytoskeletal organization, and the mechanism may participate in monocyte adherence to the arterial wall in the initiation of atherosclerosis.-Asai, A., F. Okajima, K. Nakagawa, D. Ibusuki, K. Tanimura, Y. Nakajima, M. Nagao, M. Sudo, T. Harada, T. Miyazawa, and S. Oikawa. Phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to intracellular adhesion molecule-1. J. Lipid Res. 2009. 50: 957-965. Supplementary key words lipid oxidationOxidative lipid modifications play important roles in the pathogenesis of atherosclerosis (1-4). Among oxidatively modified lipids, phosphatidylcholine hydroperoxide (PCOOH), a primary oxidation product of phosphatidylcholine (PC), was observed to be accumulated in arterial walls and blood plasma in atherosclerotic rabbits (5). PCOOH was also identified in human atherosclerotic lesions (6, 7). Furthermore, PCOOH accumulation in plasma has been shown in human subjects with pathological conditions such as hyperlipidemia (8, 9), diabetes (10), uremia (9), and alcoholism (11). Because hyperlipidemia and diabetes are strongly associated with increased incidence of atherosclerosis (12-14), higher plasma PCOOH conditions in these patients may be involved in atherogenesis.In the course of phospholipid oxidation, PC is primarily oxidized to PCOOH. Further oxidative modification of PCOOH yields various secondary oxidation products. To date, a number of the secondary oxidation products have been reported to mediate several atherogenic processes (15, 16). For instance, a series of oxidized PCs with a truncated sn-2 acyl group (sn-2-truncated PCs), such as 1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC) and 1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphocholine, activate aortic endothelial cell binding to monocytes (17-19). The sn-2-truncated PCs with a terminal aldehyde gr...

“…These results indicate that plasma PCOOH levels are strongly dependent on lipid mass or lipoprotein particle number. Therefore, patients with hyperlipidemia might be exposed to oxidative stress via lipid peroxidation as shown by the relationship between hyperlipidemia and oxidation products (28), and be in the process of developing atherosclerotic diseases through changes to the vascular antioxidant system (29) Piotrowski et al (30) have shown that human atherosclerotic lesions contain peroxidized phosphatidylcholine as a major lipid peroxide. Our study demonstrated similar results in that the atherosclerotic aorta contained large amounts of PCOOH, and the contents correlated with the extent of the lesions (Fig.…”

Section: Discussionmentioning

confidence: 99%

Fructose Ingestion Enhances Atherosclerosis and Deposition of Advanced Glycated End-products in Cholesterol-fed Rabbits

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et al. 2005

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This study was performed to investigate whether the plasma concentration of phosphatidylcholine hydroperoxide (PCOOH), which is a marker of oxidized stress in the blood, increased in cholesterol-fed rabbits, and fructose ingestion promoted this process and aggravated atherosclerosis. Male Japanese white rabbits (age: 12 weeks, and body weight: around 2.0 kg, n = 15) were divided into three groups, (1) a NN group as a normal control fed a standard diet (n = 5), (2) a CN group fed 1.0% cholesterol, and (3) a CF group given both 1.0% cholesterol and 10% fructose-containing tap water. During 8 weeks, plasma PCOOH levels increased significantly in the CN and CF groups compared to the NN group and fructose further raised the PCOOH level. The atherosclerosis was significantly promoted and the deposition of advanced glycation end products (AGEs) was marked in the CF group compared to the CN group. Fructose worsened the atheromatous lesions caused by cholesterol feeding. The mechanism is most likely through lipid peroxidation, which was increased by cholesterol feeding-induced hyperlipidemia, and the formation of AGEs. J Atheroscler Thromb, 2005; 12: 260-267.

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