Lipoprotein-associated phospholipase A2 decreases oxidized lipoprotein cellular association by human macrophages and hepatocytes

Yang, Ming; Chu, Eugene M.; Edelstein, Celina; Scanu, Angelo M.; Hill, John S.

doi:10.1016/j.bbalip.2009.10.011

Cited by 7 publications

(6 citation statements)

References 34 publications

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“…Liposomes prepared from oxLDL lipids could bind to macrophages and also compete for the binding of intact oxLDL and solubilized ApoB from oxLDL, while lipopsomes containing oxPAPC as well as a conjugate of POVPC with serum albumin proved effective competitors for the binding of intact oxLDL and oxLDL lipids ( 17,18,20 ). A monoclonal antibody against oxidized phospholipids that could recognize oxPAPC and POVPC, caused a great and hepatocytes by approximately 30-40% ( 47 ). These results are close to those found in our study.…”

Section: Discussionsupporting

confidence: 80%

Implication of lipoprotein associated phospholipase A2 activity in oxLDL uptake by macrophages

Markakis

Koropouli

Grammenou-Savvoglou

et al. 2010

Journal of Lipid Research

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Supplementary key words oxidized 1-palmitoyl-2-arachidonoyl-phosphatidylcholine • lysophosphatidylcholine • moderately oxidized LDL • heavily oxidized LDL Oxidation of LDL is considered as a prerequisite event in the atherogenic process. LDL oxidation is mediated by endothelial cells, smooth muscle cells, and macrophages in the arterial intima and oxidized LDL (oxLDL) are found in abundance into atherosclerotic lesions ( 1-6 ). Oxidative modifi cation of LDL includes i ) peroxidation of the lipids, ii ) conversion of PC to lysophosphatidylcholine ( lysoPC) (up to 50% depending on the extension of the oxidation), iii ) an increase in density, iv ) an increase in net negative charge resulting in increased electrophoretic mobility, v ) breakdown of apolipoprotein B (ApoB) into smaller peptides, and vi ) binding of oxidized lipids on ApoB ( 2,7,8 ). Oxidation of LDL has various atherogenic effects such as increased uptake by macrophages and smooth muscle cells leading to foam cell formation, increased production of adhesion molecules, induction of monocytes/macrophages and smooth muscle cell prolif-

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Section: Discussionsupporting

confidence: 80%

Implication of lipoprotein associated phospholipase A2 activity in oxLDL uptake by macrophages

Markakis

Koropouli

Grammenou-Savvoglou

et al. 2010

Journal of Lipid Research

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“…Both pharmacologic and genetic depletion of Lp-PLA 2 in minimally modifi ed lipoproteins enhanced monocyte adhesion to aortic endothelial cells compared with minimally modifi ed lipoproteins that expressed normal activity levels ( 88 ). Similarly, exogenous Lp-PLA 2 reduced cellular uptake of oxidized LDL and Lp(a), and cholesterol accumulation by monocyte-derived macrophages, compared with parallel assays conducted with inactive enzyme ( 89 ). These results suggest that the enzymatic activity of Lp-PLA 2 limits monocyte recruitment and foam cell formation within atherosclerotic lesions ( 89 ).…”

Section: Lp-pla 2 Expression In Apparently Healthy Subjectsmentioning

confidence: 64%

Modulation of oxidative stress, inflammation, and atherosclerosis by lipoprotein-associated phospholipase A2

Rosenson

Stafforini

2012

Journal of Lipid Research

152

117

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“…Many early studies have considered that (Elkind, Tai, Coates, Paik, & Sacco, ; Lp‐PLA(2) Studies Collaboration et al, ; Oei et al, ) Lp‐PLA2 can hydrolyze platelet‐activating factors, inhibit thrombosis and alleviate inflammation, and work against atherosclerosis. At present, it has been considered that (Alkuraishy et al, ; Yang et al, ) some kinds of Lp‐PLA2 that can bind with high density lipoprotein (HDL) can hydrolyze oxidized phospholipids in blood, reduce the accumulation of inflammatory mediators in phagocytes, and inhibit foam cell formation, thereby exerting anti‐inflammatory and anti‐atherosclerotic effects. In the process of the hydrolysis of oxidized low‐density lipoprotein (ox‐LDL), sLp‐PLA2 produces oxidized free fatty acids (ox‐FFA) and lysolecithin (lyso‐PC) (Bonnefont‐Rousselot, ; Ulrich et al, ).…”

Section: Discussionmentioning

confidence: 99%

Effects of dl‐3‐n‐butylphthalide on serum lipoprotein‐associated phospholipase A2 and hypersensitive C‐reactive protein levels in acute cerebral infarction

Zhang¹,

Dong²,

Liu³

et al. 2019

Brain and Behavior

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ObjectiveThis study aims to explore the curative effect of dl‐3‐n‐butylphthalide (NBP) on patients with acute cerebral infarction (ACI) and its effects on serum lipoprotein‐associated phospholipase A2 (Lp‐PLA2) and hypersensitive C‐reactive protein (hs‐CRP) levels.MethodsA total of 136 ACI patients treated in our hospital, who met the criteria, were selected and randomly divided into two groups: control group (n = 60, including 28 males and 32 females) and treatment group (n = 76, including 32 males and 44 females). Patients in the control group were treated with routine drug therapy, while patients in the treatment group were treated with NBP on this basis. A dose of 100 ml was administered by intravenous injection for 2 times/day, for 14 days. The curative effect was evaluated using the National Institute of Health Stroke Scale (NIHSS) and Barthel index (BI) self‐care ability. The levels of the two factors in serum were measured using enzyme‐linked immunosorbent assay, and the changes in levels of these two factors in serum at different time points before and after treatment were compared between the two groups.Results(a) Lp‐PLA2 and hs‐CRP levels in the treatment group after treatment were significantly lower than those before treatment and those in the control group after treatment (p < .05). (b) The NIHSS and BI scores in the treatment group were significantly lower after treatment than before treatment and those in the control group after treatment (p < .05).ConclusionDl‐3‐n‐butylphthalide can improve the expression of Lp‐PLA2 and hs‐CRP in serum in ACI patients. Furthermore, NBP has significant efficacy in inhibiting inflammation and improving neurological symptoms.

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Lipoprotein-associated phospholipase A2 decreases oxidized lipoprotein cellular association by human macrophages and hepatocytes

Cited by 7 publications

References 34 publications

Implication of lipoprotein associated phospholipase A2 activity in oxLDL uptake by macrophages

Implication of lipoprotein associated phospholipase A2 activity in oxLDL uptake by macrophages

Modulation of oxidative stress, inflammation, and atherosclerosis by lipoprotein-associated phospholipase A2

Effects of dl‐3‐n‐butylphthalide on serum lipoprotein‐associated phospholipase A2 and hypersensitive C‐reactive protein levels in acute cerebral infarction

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