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首页> 外文期刊>Chemistry and Physics of Lipids >Proatherogenic modification of LDL by surface-bound myeloperoxidase
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Proatherogenic modification of LDL by surface-bound myeloperoxidase

机译：表面结合的髓过氧化物酶对LDL的促动脉粥样硬化的修饰

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摘要

One of the factors promoting oxidative/halogenating modification of low-density lipoproteins (LDL) is myeloperoxidase (MPO). We have shown previously that MPO binds to the LDL surfaces. The LDL-MPO complex is uncoupled in the presence of peptide EQIQDDCTGDED that corresponds to a fragment of apoB-100 (445-456). In this paper we studied how this peptide, as well as inhibitors and modulators of halogenating activity of MPO such as ceruloplasmin (CP), 4-aminobenzoic acid hydrazide (ABAH) and thiocyanate (SCN~-) affect the accumulation of cholesterol and its esters in monocytes/macrophages after incubation with LDL subjected to different kinds of MPO-dependent oxidative/halogenating modification. In the presence of H_2O_2 and halides MPO causes stronger proatherogenic modification of LDL than exogenous reactive halogen species (HOCl and HOBr). Both monocytes, which differentiate into macrophages, and neutrophils secrete MPO in response to the presence of damaged LDL. The peptide EQIQDDCTGDED preventing interaction between MPO and LDL reduces the uptake of modified LDL and MPO by mono-cytes/macrophages and thus precludes the accumulation of intracellular cholesterol. Our results indicate that binding to MPO is important for LDL to become modified and acquire proatherogenic properties. The peptide EQIQDDCTGDED, CP, ABAH, and SCN~- can play the role of anti-atherogenic factors reducing the deleterious effect of catalytically active MPO on LDL and accumulation of cholesterol in macrophages.
机译：促进低密度脂蛋白（LDL）氧化/卤化修饰的因素之一是髓过氧化物酶（MPO）。先前我们已经证明MPO绑定到LDL表面。在对应于apoB-100片段（445-456）的肽EQIQDDCTGDED存在下，LDL-MPO复合物解偶联。在本文中，我们研究了该肽以及MPO的卤化活性的抑制剂和调节剂，如铜蓝蛋白（CP），4-氨基苯甲酸酰肼（ABAH）和硫氰酸盐（SCN〜-）如何影响胆固醇及其酯的积累与低密度脂蛋白孵育后，单核细胞/巨噬细胞中的单核细胞受到不同类型的MPO依赖性氧化/卤化修饰。在H_2O_2和卤化物存在下，MPO会比外源性活性卤素（HOCl和HOBr）引起LDL的更强的促动脉粥样硬化改性。分化为巨噬细胞的两个单核细胞和中性粒细胞均响应受损LDL的存在而分泌MPO。防止MPO和LDL之间相互作用的肽EQIQDDCTGDED减少了单细胞/巨噬细胞对修饰的LDL和MPO的摄取，从而阻止了细胞内胆固醇的积累。我们的结果表明，与MPO结合对于LDL的修饰和获得促动脉粥样硬化特性很重要。肽EQIQDDCTGDED，CP，ABAH和SCN〜-可以起到抗动脉粥样硬化因子的作用，降低催化活性MPO对LDL的有害作用和胆固醇在巨噬细胞中的积累。

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