Arg123-Tyr166 domain of human ApoA-I is critical for HDL-mediated inhibition of macrophage homing and early atherosclerosis in mice

Arteriosclerosis, Thrombosis, and Vascular Biology

Volumn 21, Issue 12, 2001, Pages 1977-1983

  Holvoet, Paul ^a   Peeters, Kathleen ^a   Lund Katz, Sissel ^a   Mertens, Ann ^a   Verhamme, Peter ^a   Quarck, Rozenn ^a   Stengel, Dominique ^a   Lox, Marleen ^a   Deridder, Els ^a   Bernar, Hilde ^a   Nickel, Margaret ^a   Theilmeier, Gregor ^a   Ninio, Ewa ^a   Phillips, Michael C ^a  

^a UNIVERSITY OF LEUVEN   (Belgium)

Author keywords

Apolipoprotein A I; Atherosclerosis; HDL; Macrophage homing; Oxidative stress

Indexed keywords

APOLIPOPROTEIN A1; ARGININE; HIGH DENSITY LIPOPROTEIN; TYROSINE;

ANIMAL CELL; ANIMAL EXPERIMENT; ARTICLE; ATHEROSCLEROSIS; CHOLESTEROL BLOOD LEVEL; CORONARY RISK; KNOCKOUT MOUSE; MACROPHAGE MIGRATION; MOUSE; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL;

EID: 0035569887     PISSN: 10795642     EISSN: None     Source Type: Journal    
DOI: 10.1161/hq1201.100221     Document Type: Article

References (41)

1. High-density lipoprotein: The clinical implications of recent studies
2. Plasma apolipoprotein A-1 absence associated with a marked reduction of high density lipoproteins and premature coronary artery disease
3. High levels of human apolipoprotein A-I in transgenic mice result in increased plasma levels of small high density lipoprotein (HDL) particles comparable to human HDL3
4. Expression of human apolipoprotein A-I in transgenic mice results in reduced plasma levels of murine apolipoprotein A-I and the appearance of two new high density lipoprotein size subclasses
5. Role of the carboxy-terminal domain of human apolipoprotein AI in high-density-lipoprotein metabolism: A study based on deletion and substitution variants in transgenic mice
6. Dietary fat increases high density lipoprotein (HDL) levels both by increasing the transport rates, decreasing the fractional catabolic rates of HDL cholesterol ester, apolipoprotein (Apo) A-I: Presentation of a new animal model and mechanistic studies in human Apo A-I transgenic and control mice
7. Inhibition of early atherogenesis in transgenic mice by human apolipoprotein AI
8. Severe hypercholesterolemia and atherosclerosis in apolipoprotein E-deficient mice created by homologous recombination in ES cells
9. Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E
10. ApoE-deficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree
11. Atherosclerosis in mice lacking apo E: Evaluation of lesional development and progression
12. Apolipoprotein AI transgene corrects apolipoprotein E deficiency-induced atherosclerosis in mice
13. Human apolipoprotein A-I gene expression increases high density lipoprotein and suppresses atherosclerosis in the apolipoprotein E-deficient mouse
14. Atherosclerosis in transgenic mice overexpressing apolipoprotein A-II
15. Expression of human apolipoprotein A-II and its effect on high density lipoproteins in transgenic mice
16. Functional lecithin:cholesterol acyltransferase deficiency and high density lipoprotein deficiency in transgenic mice overexpressing human apolipoprotein A-II
17. Protein composition determines the anti-atherogenic properties of HDL in transgenic mice
18. Role of the Arg123-Tyr166 paired helix of apolipoprotein A-I in lecithin:cholesterol acyltransferase activation
19. The Arg123-Tyr166 central domain of human apoAI is critical for lecithin:cholesterol acyltransferase-induced hyperalphalipoproteinemia and HDL remodeling in transgenic mice
20. Malondialdehyde-modified low density lipoproteins in patients with atherosclerotic disease
21. ApoE-deficient mice are a model of lipoprotein oxidation in atherogenesis: Demonstration of oxidation-specific epitopes in lesions and high titers of autoantibodies to malondialdehyde-lysine in serum
22. PAF-degrading acetylhydrolase is preferentially associated with dense LDL and VHDL-1 in human plasma: Catalytic characteristics and relation to the monocyte-derived enzyme
23. Inhibition of alpha4 integrin and ICAM-1 markedly attenuate macrophage homing to atherosclerotic plaques in apoE-deficient mice
24. HDL-associated PAF-AH reduces endothelial adhesiveness in apoE-/- mice
25. Induction of tumor formation and cell transformation by polyoma middle T antigen in the absence of Src
26. Circulating activated platelets assist THP-1 monocytoid/endothelial cell interaction under shear stress
27. Efflux of cellular cholesterol and phospholipid to lipid-free apolipoproteins and class A amphipathic peptides
28. Substitution of the carboxyl-terminal domain of apo AI with apo AII sequences restores the potential of HDL to reduce the progression of atherosclerosis in apo E knockout mice
29. Adenovirus-mediated gene transfer of human platelet-activating factor-acetylhydrolase prevents injury-induced neointima formation and reduces spontaneous atherosclerosis in apolipoprotein E-deficient mice
30. High density lipoprotein phospholipid composition is a major determinant of the bi-directional flux and net movement of cellular free cholesterol mediated by scavenger receptor BI
31. Cholesterol efflux, lecithin-cholesterol acyltransferase activity, and pre-beta particle formation by serum from human apolipoprotein A-I and apolipoprotein A-I/apolipoprotein A-II transgenic mice consistent with the latter being less effective for reverse cholesterol transport
32. Effects of deletion of the carboxyl-terminal domain of ApoA-I or of its substitution with helices of ApoA-II on in vitro and in vivo lipoprotein association
33. Cholesterol efflux potential of sera from mice expressing human cholesteryl ester transfer protein and/or human apolipoprotein AI
34. Effects of recombinant apolipoprotein A-I(Milano) on aortic atherosclerosis in apolipoprotein E-deficient mice
35. Overexpression of apolipoprotein AII in transgenic mice converts high density lipoproteins to proinflammatory particles
36. Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoprotein: Step 1
37. Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoprotein: Steps 2 and 3
38. High-density lipoproteins inhibit cytokine-induced expression of endothelial cell adhesion molecules
39. Human serum paraoxonase/arylesterase's retained hydrophobic N-terminal leader sequence associates with HDLs by binding phospholipids: Apolipoprotein A-I stabilizes activity
40. Cysteine substitutions in apolipoprotein A-I primary structure modulate paraoxonase activity
41. A novel lecithin-cholesterol acyltransferase antioxidant activity prevents the formation of oxidized lipids during lipoprotein oxidation