beta(2) integrin-dependent neutrophil adhesion induced by minimally modified low-density lipoproteins is mainly mediated by F-2-isoprostanes

Article

关键词: IN-VIVO;    LIPID-PEROXIDATION;    OXIDATIVE STRESS;    ISOPROSTANES;    ANGIOPLASTY;    RESTENOSIS;    F2-ALPHA;    ATHEROSCLEROSIS;    INFLAMMATION;    GENERATION;   

DOI  :  10.1161/01.CIR.0000037223.92135.38

来源: SCIE

【 摘 要 】

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 A(2) 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.

【 授权许可】

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