由轻度修饰的低密度脂蛋白诱导的β2整合素依赖性中性粒细胞黏附主要由F2-异前列腺素介导。
Beta2 integrin-dependent neutrophil adhesion induced by minimally modified low-density lipoproteins is mainly mediated by F2-isoprostanes.
作者信息
Fontana Luigi, Giagulli Cinzia, Cominacini Luciano, Pasini Anna Fratta, Minuz Pietro, Lechi Alessandro, Sala Angelo, Laudanna Carlo
机构信息
Department of Medicine, University of Verona, Italy.
出版信息
Circulation. 2002 Nov 5;106(19):2434-41. doi: 10.1161/01.cir.0000037223.92135.38.
BACKGROUND
Oxidation of LDL produces a series of biologically active, oxidized lipids. Among them, isoprostanes, and in particular iPF(2alpha)-III, seem to be crucial in mediating some of the key cellular events seen in myocardial ischemia-reperfusion injury.
METHODS AND RESULTS
Minimally modified LDL (MM-LDL) triggers a dose-dependent, very rapid neutrophil adhesion to human fibrinogen. Rapid adhesion triggering correlates with degree of LDL oxidation and accumulation of isoprostanes. Isoprostanes accumulated in MM-LDL are major determinants of the proadhesive effect of oxidized LDL, as shown by experiments of receptor functional deletion. Moreover, evidence is provided of expression on human neutrophils of a biological active isoprostane receptor distinct from the classical thromboxane A2 receptor.
CONCLUSIONS
These data suggest that isoprostanes are major contributors to the proadhesive effect induced by MM-LDL on neutrophils and provide additional evidence for the involvement of isoprostanes in the pathogenesis of myocardial ischemia/reperfusion injury.
背景
低密度脂蛋白（LDL）的氧化会产生一系列具有生物活性的氧化脂质。其中，异前列腺素，尤其是iPF(2α)-III，似乎在介导心肌缺血再灌注损伤中一些关键的细胞事件中起着至关重要的作用。
方法与结果
轻度修饰的LDL（MM-LDL）会引发剂量依赖性的、非常快速的中性粒细胞与人纤维蛋白原的黏附。快速的黏附引发与LDL氧化程度和异前列腺素的积累相关。如受体功能缺失实验所示，MM-LDL中积累的异前列腺素是氧化LDL促黏附作用的主要决定因素。此外，有证据表明人类中性粒细胞上存在一种不同于经典血栓素A2受体的生物活性异前列腺素受体。
结论
这些数据表明异前列腺素是MM-LDL诱导的中性粒细胞促黏附作用的主要促成因素，并为异前列腺素参与心肌缺血/再灌注损伤的发病机制提供了额外证据。
Zotero 插件