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Research Paper Low-density lipoprotein modified by myeloperoxidase oxidants induces endothelial dysfunction

机译：研究论文髓过氧化物酶氧化剂修饰的低密度脂蛋白诱导内皮功能障碍

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Low-density lipoprotein (LDL) modified by hypochlorous acid (HOCl) produced by myeloperoxidase (MPO) is present in atherosclerotic lesions, where it is implicated in the propagation of inflammation and acceleration of lesion development by multiple pathways, including the induction of endothelial dysfunction. Thiocyanate (SCN-) ions are utilised by MPO to produce the oxidant hypothiocyanous acid (HOSCN), which reacts with LDL in a different manner to HOCl. Whilst the reactivity of HOCl-modified LDL has been previously studied, the role of HOSCN in the modification of LDL in vivo is poorly defined, although emerging evidence suggests that these particles have distinct biological properties. This is important because elevated plasma SCN- is linked with both the propagation and prevention of atherosclerosis. In this study, we demonstrate that both HOSCN- and HOCl-modified LDL inhibit endothelium-mediated vasorelaxation ex vivo in rat aortic ring segments. In vitro experiments with human coronary artery endothelial cells show that HOSCN-modified LDL decreases in the production of nitric oxide (NO?) and induces the loss of endothelial nitric oxide synthase (eNOS) activity. This occurs to a similar extent to that seen with HOCl-modified LDL. In each case, these effects are related to eNOS uncoupling, rather than altered expression, phosphorylation or cellular localisation. Together, these data provide new insights into role of MPO and LDL modification in the induction of endothelial dysfunction, which has implications for both the therapeutic use of SCN- within the setting of atherosclerosis and for smokers, who have elevated plasma levels of SCN-, and are more at risk of developing cardiovascular disease.
机译：髓过氧化物酶（MPO）产生的由次氯酸（HOCl）修饰的低密度脂蛋白（LDL）存在于动脉粥样硬化病变中，在其中涉及炎症的传播和通过多种途径加速病变发展，包括诱导内皮功能障碍。 MPO利用硫氰酸盐（SCN -）离子产生氧化剂次硫氰酸（HOSCN），该氧化剂与LDL的反应方式与HOCl不同。尽管以前已经研究了HOCl修饰的LDL的反应性，但是对HOSCN在体内LDL修饰中的作用的定义尚不明确，尽管新兴证据表明这些颗粒具有独特的生物学特性。这很重要，因为血浆SCN -升高与动脉粥样硬化的传播和预防有关。在这项研究中，我们证明，HOSCN和HOCl修饰的LDL均可在大鼠主动脉环段中抑制内皮介导的血管舒张。人冠状动脉内皮细胞的体外实验表明，HOSCN修饰的LDL减少了一氧化氮（NO ？）的产生，并诱导内皮一氧化氮合酶（eNOS）活性降低。这发生的程度与HOCl修饰的LDL相似。在每种情况下，这些效应都与eNOS的解偶联有关，而不是与表达，磷酸化或细胞定位改变有关。总之，这些数据为MPO和LDL修饰在诱导内皮功能障碍中的作用提供了新的见解，这对动脉粥样硬化背景下SCN -的治疗用途和吸烟者都有影响。 SCN -的血浆水平升高，更容易患上心血管疾病。

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