2009
DOI: 10.1074/jbc.m109.047605
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Modification of High Density Lipoprotein by Myeloperoxidase Generates a Pro-inflammatory Particle

Abstract: High density lipoprotein (HDL) is the major atheroprotective particle in plasma. Recent studies demonstrate that myeloperoxidase (MPO) binds to HDL in vivo, selectively targeting apolipoprotein A1 (apoA1) of HDL for oxidative modification and concurrent loss in cholesterol efflux and lecithin cholesterol acyl transferase activating activities, generating a "dysfunctional HDL" particle. We now show that (patho)physiologically relevant levels of MPO-catalyzed oxidation result in loss of noncholesterol efflux act… Show more

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Cited by 238 publications
(192 citation statements)
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References 58 publications
(54 reference statements)
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“…137 Besides functional consequences for cellular cholesterol efflux and reverse cholesterol transport, exposure of human HDL to the MPO/H2O2/Cl -system has also been found to ablate the ability of HDL to suppress serum starvation-induced capase-3 activation and thereby apoptosis in endothelial cells and to promote eNOS activation. 133 Furthermore, HDL modified by MPO enhanced rather than inhibited the protein expression of VCAM-1 on endothelial cells treated with TNF-α. 133 The loss of anti-apoptotic and anti-inflammatory functions of HDL following MPO treatment has been explained by the inability of MPO-oxidized HDL to bind to SR-BI.…”
Section: Myeloperoxidase-mediated Protein Modificationsmentioning
confidence: 95%
See 3 more Smart Citations
“…137 Besides functional consequences for cellular cholesterol efflux and reverse cholesterol transport, exposure of human HDL to the MPO/H2O2/Cl -system has also been found to ablate the ability of HDL to suppress serum starvation-induced capase-3 activation and thereby apoptosis in endothelial cells and to promote eNOS activation. 133 Furthermore, HDL modified by MPO enhanced rather than inhibited the protein expression of VCAM-1 on endothelial cells treated with TNF-α. 133 The loss of anti-apoptotic and anti-inflammatory functions of HDL following MPO treatment has been explained by the inability of MPO-oxidized HDL to bind to SR-BI.…”
Section: Myeloperoxidase-mediated Protein Modificationsmentioning
confidence: 95%
“…133 Furthermore, HDL modified by MPO enhanced rather than inhibited the protein expression of VCAM-1 on endothelial cells treated with TNF-α. 133 The loss of anti-apoptotic and anti-inflammatory functions of HDL following MPO treatment has been explained by the inability of MPO-oxidized HDL to bind to SR-BI. 133 However, our lab did not find any reduced binding of HDL from CAD patients with endothelial dysfunction.…”
Section: Myeloperoxidase-mediated Protein Modificationsmentioning
confidence: 95%
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“…34 MPO-modified HDL cannot bind to the HDL receptor and scavenger receptor B1, and promote proinflammatory activities such as upregulation of nuclear factor (NF)-κB and expression of adhesion molecules by ECs. 82 Furthermore, both modified HDL and ApoA1 become immunogenic because modification creates new epitopes that could be recognized by immune cells and induce humoral immune response and anti-ApoA1 antibody production.…”
Section: Role Of Modified Apoa1 In Atherosclerosismentioning
confidence: 99%