Dataset related to the article "Relationship Between Plasma Osteopontin and Arginine Pathway Metabolites in Patients With Overt Coronary Artery Disease"

This record contains raw data related to the article "Relationship Between Plasma Osteopontin and Arginine Pathway Metabolites in Patients With Overt Coronary Artery Disease" ABSTRACT <strong>Introduction: </strong>Osteopontin (OPN) is involved in ectopic calcification. Its circulating form is upregulated in coronary artery disease (CAD) patients. Circulating OPN levels positively correlate with oxidative stress, one of the major triggers of endothelial dysfunction. Endothelial dysfunction is, in turn, associated with reduced nitric oxide (NO) bioavailability due to the impaired arginine pathway. The aim of this study was to better understand the correlations between OPN, oxidative stress markers, and the arginine pathway metabolites. <strong>Methods and results: </strong>ELISA and mass spectrometry techniques have been used to evaluate circulating OPN and arginine pathway/oxidative stress metabolites, respectively, in twenty-five control subjects and thirty-three patients with overt atherosclerosis. OPN positively correlates with 2,3-dinor-8isoPGF2a levels (<em>p</em> = 0.02), ornithine (<em>p</em> = 0.01), ADMA (<em>p</em> = 0.001), SDMA (<em>p</em> = 0.03), and citrulline (<em>p</em> = 0.008) levels only in CAD patients. In addition, citrulline positively correlated with ADMA (<em>p</em> = 0.02) levels, possibly as result of other sources of citrulline biosynthetic pathways. <strong>Conclusion: </strong>The association between OPN and impaired arginine/NO pathway could play a role in the inhibition of endothelial NO synthase (eNOS) and/or in the arginase activation in the context of CAD patients. However, further studies are needed to verify the cause-effect relationship between OPN, oxidative stress, and arginine/NO pathway dysregulation.本数据集包含与题为《显性冠状动脉疾病患者血浆骨桥蛋白（Osteopontin, OPN）与精氨酸通路代谢物的相关性》的学术论文相关的原始数据。 <strong>引言：</strong>骨桥蛋白（Osteopontin, OPN）参与异位钙化过程，其循环形式在冠状动脉疾病（coronary artery disease, CAD）患者体内表达上调。循环OPN水平与氧化应激呈正相关，而氧化应激是诱发内皮功能障碍的主要因素之一。反过来，内皮功能障碍与精氨酸通路受损导致的一氧化氮（nitric oxide, NO）生物利用度降低密切相关。本研究旨在进一步阐明OPN、氧化应激标志物与精氨酸通路代谢物之间的关联。 <strong>方法与结果：</strong>本研究分别采用酶联免疫吸附测定（ELISA）与质谱技术，对25名对照受试者及33名显性动脉粥样硬化患者的循环OPN与精氨酸通路/氧化应激代谢物进行检测。仅在CAD患者中，OPN水平与2,3-二去甲-8-异前列腺素F2α（2,3-dinor-8isoPGF2a，<em>p</em> = 0.02）、鸟氨酸（ornithine，<em>p</em> = 0.01）、不对称二甲基精氨酸（asymmetric dimethylarginine, ADMA，<em>p</em> = 0.001）、对称二甲基精氨酸（symmetric dimethylarginine, SDMA，<em>p</em> = 0.03）以及瓜氨酸（citrulline，<em>p</em> = 0.008）水平呈正相关。此外，瓜氨酸与ADMA（<em>p</em> = 0.02）水平呈正相关，这可能与瓜氨酸生物合成通路的其他来源有关。 <strong>结论：</strong>在CAD患者中，OPN与精氨酸/NO通路受损之间的关联，可能在内皮型一氧化氮合酶（endothelial NO synthase, eNOS）抑制和/或精氨酸酶激活过程中发挥作用。不过，仍需开展进一步研究以验证OPN、氧化应激与精氨酸/NO通路失调之间的因果关系。