Effects of Myeloperoxidase-Induced Oxidation on Antiatherogenic Functions of High-Density Lipoprotein.

IF 5.9 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Journal of Lipids Pub Date : 2015-01-01 Epub Date: 2015-07-14 DOI:10.1155/2015/592594
Takahiro Kameda, Ryunosuke Ohkawa, Kouji Yano, Yoko Usami, Akari Miyazaki, Kazuyuki Matsuda, Kenji Kawasaki, Mitsutoshi Sugano, Tetsuo Kubota, Minoru Tozuka
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引用次数: 20

Abstract

High-density lipoprotein (HDL) has protective effects against the development of atherosclerosis; these effects include reverse cholesterol transport, antioxidant ability, and anti-inflammation. Myeloperoxidase (MPO) secreted by macrophages in atherosclerotic lesions generates tyrosyl radicals in apolipoprotein A-I (apoA-I) molecules, inducing the formation of apoA-I/apoA-II heterodimers through the tyrosine-tyrosine bond in HDL. Functional characterization of HDL oxidized by MPO could provide useful information about the significance of apoA-I/apoA-II heterodimers measurement. We investigated the effects of MPO-induced oxidation on the antiatherogenic functions of HDL as described above. The antioxidant ability of HDL, estimated as the effect on LDL oxidation induced by copper sulfate, was not significantly affected after MPO oxidation. HDL reduced THP-1 monocyte migration by suppressing the stimulation of human umbilical vein endothelial cells induced by lipopolysaccharide (LPS). MPO-oxidized HDL also showed inhibition of THP-1 chemotaxis, but the extent of inhibition was significantly attenuated compared to intact HDL. MPO treatment did not affect the cholesterol efflux capacity of HDL from [(3)H]-cholesterol-laden macrophages derived from THP-1 cells. The principal effect of MPO oxidation on the antiatherogenic potential of HDL would be the reduction of anti-inflammatory ability, suggesting that measurement of apoA-I/apoA-II heterodimers might be useful to estimate anti-inflammatory ability of HDL.

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髓过氧化物酶诱导氧化对高密度脂蛋白抗动脉粥样硬化功能的影响。
高密度脂蛋白(HDL)对动脉粥样硬化的发生具有保护作用;这些作用包括逆向胆固醇运输、抗氧化能力和抗炎症。动脉粥样硬化病变中巨噬细胞分泌的髓过氧化物酶(MPO)在载脂蛋白A-I (apoA-I)分子中产生酪氨酸自由基,通过HDL中的酪氨酸-酪氨酸键诱导形成apoA-I/apoA-II异源二聚体。MPO氧化HDL的功能表征可以为apoA-I/apoA-II异源二聚体的测定提供有用的信息。如上所述,我们研究了mpo诱导的氧化对HDL抗动脉粥样硬化功能的影响。MPO氧化对HDL的抗氧化能力无显著影响,以硫酸铜对LDL氧化的影响来评价。HDL通过抑制脂多糖(LPS)对人脐静脉内皮细胞的刺激来减少THP-1单核细胞的迁移。mpo氧化的HDL也表现出对THP-1趋化性的抑制,但与完整的HDL相比,抑制程度明显减弱。MPO处理不影响THP-1细胞衍生的[(3)H]-胆固醇巨噬细胞中HDL的胆固醇外排能力。MPO氧化对HDL抗动脉粥样硬化潜力的主要影响是降低抗炎能力,这表明测量apoA-I/apoA-II异源二聚体可能有助于估计HDL的抗炎能力。
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来源期刊
Journal of Lipids
Journal of Lipids BIOCHEMISTRY & MOLECULAR BIOLOGY-
自引率
0.00%
发文量
7
审稿时长
12 weeks
期刊介绍: Journal of Lipids is a peer-reviewed, Open Access journal that publishes original research articles and review articles related to all aspects of lipids, including their biochemistry, synthesis, function in health and disease, and nutrition. As an interdisciplinary journal, Journal of Lipids aims to provide a forum for scientists, physicians, nutritionists, and other relevant health professionals.
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