scholarly journals Folic Acid Supplementation Delays Atherosclerotic Lesion Development by Modulating MCP1 and VEGF DNA Methylation Levels In Vivo and In Vitro

2017 ◽  
Vol 18 (5) ◽  
pp. 990 ◽  
Author(s):  
Shanshan Cui ◽  
Wen Li ◽  
Xin Lv ◽  
Pengyan Wang ◽  
Yuxia Gao ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Folic Acid ◽  
Atherosclerotic Lesion ◽  
Folic Acid Supplementation ◽  
Lesion Development ◽  
Acid Supplementation ◽  
Atherosclerotic Lesion Development

Folic acid supplementation delays atherosclerotic lesion development in apoE-deficient mice

Life Sciences ◽  
2007 ◽  
Vol 80 (7) ◽  
pp. 638-643 ◽  
Author(s):  
Ricardo Carnicer ◽  
María A. Navarro ◽  
José M. Arbonés-Mainar ◽  
Sergio Acín ◽  
Mario A. Guzmán ◽  
...  
Keyword(s):  
Folic Acid ◽  
Atherosclerotic Lesion ◽  
Folic Acid Supplementation ◽  
Lesion Development ◽  
Acid Supplementation ◽  
Deficient Mice ◽  
Atherosclerotic Lesion Development

Folate: In Vitro and in Vivo Effects on VLDL and LDL Oxidation

2007 ◽  
Vol 77 (1) ◽  
pp. 66-72 ◽  
Author(s):  
McEneny ◽  
Couston ◽  
McKibben ◽  
Young ◽  
Woodside
Keyword(s):  
Folic Acid ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Folic Acid Supplementation ◽  
Serum Folate ◽  
Ldl Oxidation ◽  
Low Density ◽  
Acid Supplementation

Raised total homocysteine (tHcy) levels may be involved in the etiology of cardiovascular disease and can lead to damage of vascular endothelial cells and arterial wall matrix. Folic acid supplementation can help negate these detrimental effects by reducing tHcy. Recent evidence has suggested an additional anti-atherogenic property of folate in protecting lipoproteins against oxidation. This study utilized both an in vitro and in vivo approach. In vitro: Very-low-density lipoprotein (VLDL) and low density lipoprotein (LDL) were isolated by rapid ultracentrifugation and then oxidized in the presence of increasing concentrations (0→ μmol/L) of either folic acid or 5-methyltetrahydrofolate (5-MTHF). In vivo: Twelve female subjects were supplemented with folic acid (1 mg/day), and the pre- and post-VLDL and LDL isolates subjected to oxidation. In vitro: 5-MTHF, but not folic acid, significantly increased the resistance of VLDL and LDL to oxidation. In vivo: Following folic acid supplementation, tHcy decreased, serum folate increased, and both VLDL and LDL displayed a significant increase in their resistance to oxidation. These results indicated that in vitro, only the active form of folate, 5-MTHF, had antioxidant properties. In vivo results demonstrated that folic acid supplementation reduced tHcy and protected both VLDL and LDL against oxidation. These findings provide further support for the use of folic acid supplements to aid in the prevention of atherosclerosis.

scholarly journals Analysis of Locus‐Specific DNA Methylation in Response to Chronic Folic Acid Supplementation and Withdrawal in Chinese Women

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Jason O Brant ◽  
Jiang‐Hui Zhu ◽  
Krista Crider ◽  
R J Berry ◽  
Ling Hao ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Folic Acid ◽  
Chinese Women ◽  
Folic Acid Supplementation ◽  
Acid Supplementation

scholarly journals No Effect of Folic Acid Supplementation on Global DNA Methylation in Men and Women with Moderately Elevated Homocysteine

PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e24976 ◽  
Author(s):  
Audrey Y. Jung ◽  
Yvo Smulders ◽  
Petra Verhoef ◽  
Frans J. Kok ◽  
Henk Blom ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Folic Acid ◽  
Folic Acid Supplementation ◽  
Global Dna Methylation ◽  
Men And Women ◽  
Acid Supplementation

Abstract 1721: Deletion of Both Macrophage ABCG1 and ApoE Independently Promotes Atherosclerotic Lesion Development in LDL Receptor Knockout Mice

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Ruud Out ◽  
Bart Lammers ◽  
Reeni B. Hildebrand ◽  
Carmel M. Quinn ◽  
David Williamson ◽  
...  
Keyword(s):  
Cholesterol Efflux ◽  
Ldl Receptor ◽  
Atherosclerotic Lesion ◽  
Independent Effect ◽  
High Cholesterol Diet ◽  
Moderate Increase ◽  
Lesion Development ◽  
Macrophage Cholesterol Efflux ◽  
Atherosclerotic Lesion Development

Objective ATP-binding cassette transporter G1 (ABCG1) and apolipoprotein E (apoE) play a role in macrophage cholesterol efflux and consequently the development of atherosclerosis. Although a possible interaction between ABCG1 and apoE in cholesterol efflux was postulated, the combined action of these proteins in atherosclerosis is still unclear. Methods and Results LDL receptor knockout (KO) mice were transplanted with bone marrow from ABCG1/apoE double KO (dKO) mice, their respective single knockouts, and wild-type (WT) controls. After feeding a high-fat/high-cholesterol diet for 6 weeks, no differences were found in serum lipid levels. However, the mean atherosclerotic lesion area in dKO transplanted animals (187 ± 18 × 10 3 μ m 2 ) was 1.4-fold (p < 0.01) increased compared to single knockouts (ABCG1 KO: 138 ± 5 × 10 3 μm 2 ; apoE KO: 131 ± 7 × 10 3 μm 2 ) and 1.9-fold (p< 0.001) as compared to WT controls (97 ± 15 × 10 3 μm 2 ). In vitro cholesterol efflux experiments confirmed that combined deletion of ABCG1 and apoE resulted in a larger attenuation of macrophage cholesterol efflux to HDL as compared to single knockouts. Conclusions Deletion of macrophage ABCG1 or apoE does lead to a moderate increase in atherosclerotic lesion development while combined deletion of ABCG1 and apoE induces a more dramatic increase in atherosclerosis. These results indicate an added, independent effect for both macrophage ABCG1 and apoE in atherosclerosis.

Synthesis of recombinant high density lipoprotein with apolipoprotein A-I and apolipoprotein A-V

2011 ◽  
Vol 392 (5) ◽  
Author(s):  
Xinbo Zhang ◽  
Baosheng Chen
Keyword(s):  
High Density Lipoprotein ◽  
Low Density Lipoprotein ◽  
Atherosclerotic Lesion ◽  
Density Lipoprotein ◽  
High Density ◽  
Over Expression ◽  
Apolipoprotein A ◽  
Atherosclerotic Lesion Development

Abstract It has been shown that apolipoprotein A-V (apoA-V) over-expression significantly lowers plasma triglyceride levels and decreases atherosclerotic lesion development. To assess the feasibility of recombinant high density lipoprotein (rHDL) reconstituted with apoA-V and apolipoprotein A-I (apoA-I) as a therapeutic agent for hyperlipidemic disorder and atherosclerosis, a series of rHDL were synthesized in vitro with various mass ratios of recombinant apoA-I and apoA-V. It is interesting to find that apoA-V of rHDL had no effect on lipoprotein lipase (LPL) activation in vitro and very low density lipoprotein (VLDL) clearance in HepG2 cells and in vivo. By contrast, LPL activation and VLDL clearance were inhibited by the addition of apoA-V to rHDL. Furthermore, the apoA-V of rHDL could not redistribute from rHDL to VLDL after incubation at 37°C for 30 min. These findings suggest that an increase of apoA-V in rHDL could not play a role in VLDL clearance in vitro and in vivo, which could, at least in part, attribute to the lost redistribution of apoA-V from rHDL to VLDL and LPL binding ability of apoA-V in rHDL. The therapeutic application of rHDL reconstituted with apoA-V and apoA-I might need the construction of rHDL from which apoA-V could freely redistribute to VLDL.

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