Apolipoprotein A-I Limits the Negative Effect of Tumor Necrosis Factor on Lymphangiogenesis

Bisoendial, Radjesh J.; Tabet, Fatiha; Tak, Paul P.; Petrides, Francine; Torres, Luisa; Hou, Liming; Cook, Adam J. L.; Barter, Philip J.; Weninger, Wolfgang; Rye, Kerry‐Anne

doi:10.1161/atvbaha.115.305777

Cited by 13 publications

(14 citation statements)

References 40 publications

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“…ApoA-I treatment has been demonstrated to increase podoplanin mRNA level, which could potentially help the CLEC-2/podoplanin interaction with platelets. 38 In the present study, we hypothesize that the protective effect of apoA-I is mediated at least in part by preserving collecting lymphatic vessel function by mechanisms that include modulating platelet adhesion on LECs. Our findings could bring forth a new pleiotropic role for apoA-I in lymphatic function and unveil new potential therapeutic targets for the prevention and treatment of atherosclerosis.…”

mentioning

confidence: 73%

Apolipoprotein A‐I Modulates Atherosclerosis Through Lymphatic Vessel‐Dependent Mechanisms in Mice

Milasan

Jean

Dallaire

et al. 2017

JAHA

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BackgroundSubcutaneously injected lipid‐free apoA‐I (apolipoprotein A‐I) reduces accumulation of lipid and immune cells within the aortic root of hypercholesterolemic mice without increasing high‐density lipoprotein–cholesterol concentrations. Lymphatic vessels are now recognized as prerequisite players in the modulation of cholesterol removal from the artery wall in experimental conditions of plaque regression, and particular attention has been brought to the role of the collecting lymphatic vessels in early atherosclerosis‐related lymphatic dysfunction. In the present study, we address whether and how preservation of collecting lymphatic function contributes to the protective effect of apoA‐I.Methods and ResultsAtherosclerotic Ldlr −/− mice treated with low‐dose lipid‐free apoA‐I showed enhanced lymphatic transport and abrogated collecting lymphatic vessel permeability in atherosclerotic Ldlr −/− mice when compared with albumin‐control mice. Treatment of human lymphatic endothelial cells with apoA‐I increased the adhesion of human platelets on lymphatic endothelial cells, in a bridge‐like manner, a mechanism that could strengthen endothelial cell–cell junctions and limit atherosclerosis‐associated collecting lymphatic vessel dysfunction. Experiments performed with blood platelets isolated from apoA‐I‐treated Ldlr −/− mice revealed that apoA‐I decreased ex vivo platelet aggregation. This suggests that in vivo apoA‐I treatment limits platelet thrombotic potential in blood while maintaining the platelet activity needed to sustain adequate lymphatic function.ConclusionsAltogether, we bring forward a new pleiotropic role for apoA‐I in lymphatic function and unveil new potential therapeutic targets for the prevention and treatment of atherosclerosis.

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confidence: 73%

Apolipoprotein A‐I Modulates Atherosclerosis Through Lymphatic Vessel‐Dependent Mechanisms in Mice

Milasan

Jean

Dallaire

et al. 2017

JAHA

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“…In addition, apoA-I enhances the proliferation of human endothelial progenitor cells (EPCs) and promotes angiogenesis through ATP synthase in cell surface [36]. ApoA-I restores neovascularization of the lymphatic system in tumor necrosis factor (TNF)-alpha-mediated inflammatory responses [37]. We also found that human apoA-I induces cyclooxygenase-2 (COX-2) expression and prostaglandin I-2 (PGI2) release in endothelial cells through ABCA1 [38].…”

Section: Apolipoprotein A-i (Apoa-i)mentioning

confidence: 84%

High-Density Lipoprotein: From Biological Functions to Clinical Perspectives

Liu¹

2020

Apolipoproteins, Triglycerides and Cholesterol

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High-density lipoprotein (HDL) is a heterogeneous particle composed of apolipoproteins, enzymes, and lipids. Besides transporting cholesterol to the liver, HDL also exerts many protections on anti-oxidation, anti-inflammation, and anti-apoptosis. Initial understandings of HDL came from its protective roles against atherosclerosis and the observation that high plasma HDL cholesterol (HDL-C) levels seemed to decrease cardiovascular disease (CVD) attack. However, those patients either with cholesterol ester transfer protein (CETP) deficiency or taking CETP inhibitors substantially elevated HDL-C levels but did not necessarily decrease CVD risk. Thus, some researchers suggested that quantitative measurements of HDL particle (HDL-P) might be more valuable than traditional HDL-C measurements. What is more bewildering is that HDL from patients with systemic inflammation decreased its protective effects and even became a pro-inflammatory factor. Recently, synthesized HDL and apolipoprotein mimetic peptides showed biological functions similar to native ones. Expectedly, lots of novel measurement methods and therapeutic agents about HDL would be established soon.

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“…Their main metabolic functions included lipid and glucose metabolism, transport/metabolism of vitamins and minerals, immune system function, blood clotting, and acute phase reactions (Bisoendial et al, 2015;Calder et al, 2013;Campenhout, Campenhout, & Lagrou, 2003;Carter & Worwood, 2007;Clerc et al, 2016;Dabrowska, Tarach Toonen et al, 2016;UniProt, 2016UniProt, , 2017aUniProt, , 2017bWalldius & Jungner, 2004;Wang et al, 2015;Wu & Lyons, 2011). Their main metabolic functions included lipid and glucose metabolism, transport/metabolism of vitamins and minerals, immune system function, blood clotting, and acute phase reactions (Bisoendial et al, 2015;Calder et al, 2013;Campenhout, Campenhout, & Lagrou, 2003;Carter & Worwood, 2007;Clerc et al, 2016;Dabrowska, Tarach Toonen et al, 2016;UniProt, 2016UniProt, , 2017aUniProt, , 2017bWalldius & Jungner, 2004;Wang et al, 2015;Wu & Lyons, 2011).…”

Section: Discussionmentioning

confidence: 99%

Metabo groups in response to micronutrient intervention: Pilot study

Coelho-Landell

Salomão

Almada

et al. 2019

Food Science & Nutrition

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Micronutrients and their metabolites are cofactors in proteins involved in lipid metabolism. The present study was a subproject of the Harmonized Micronutrient Project (ClinTrials.gov # NCT01823744). Twenty participants were randomly selected from 136 children and adolescents that consumed a daily dose of 12 vitamins and 5 minerals supplementation for 6 weeks. The 20 individuals were divided into two pools of 10 individuals, according to their lipid profile at baseline (Pool 1 with lower triglycerides, LDL, and VLDL). The individuals were analyzed at baseline, after 6 weeks of daily supplementation, and after 6 weeks of a washout period in relation to anthropometric, body composition, food intake, lipid profile, micronutrient levels, and iTRAQ proteomic data. Genetic ancestry and its association with vitamin serum levels were also determined. After supplementation, LDL levels decreased while alpha-tocopherol and pantothenic acid levels increased in pool 2; lipid profiles in pool 1 did not change but had higher plasma levels of pantothenic acid, pyridoxal, and pyridoxic acid. In pool 2, expression of some proteins increased, and expression of other ones decreased after intervention, while in pool 1, the same proteins responded inversely or did not change their levels. Plasma alpha-tocopherol and Native American genetic ancestry explained a significant fraction of LDL plasma levels at baseline and in response to the intervention. After intervention, changes in expression of alpha-1 antitrypsin, haptoglobin, Ig alpha-1 chain C region, plasma protease C1 inhibitor, alpha-1-acid glycoprotein 1, fibrinogen alpha, beta, and gamma-chain in individuals in pool 2 may be associated with levels of LDL and vitamin E. Vitamin E and Native American genetic ancestry may also be implicated in changes of vitamin E and LDL levels. The results of this pilot study must be validated in future studies with larger sample size or in in vitro studies. 20 participants were divided into two metabolic groups according only to their lipid profiles: individuals in pool 1 (n = 10) had lower triglycerides, LDL, and VLDL levels, and individuals in pool 2 K E Y W O R D S genetic ancestry, intervention study, lipid profile, metabolomics, proteomics, Vitamin plasma levels

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Apolipoprotein A-I Limits the Negative Effect of Tumor Necrosis Factor on Lymphangiogenesis

Cited by 13 publications

References 40 publications

Apolipoprotein A‐I Modulates Atherosclerosis Through Lymphatic Vessel‐Dependent Mechanisms in Mice

Apolipoprotein A‐I Modulates Atherosclerosis Through Lymphatic Vessel‐Dependent Mechanisms in Mice

High-Density Lipoprotein: From Biological Functions to Clinical Perspectives

Metabo groups in response to micronutrient intervention: Pilot study

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