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10.1093/eurheartj/ehv007

http://scihub22266oqcxt.onion/10.1093/eurheartj/ehv007
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C4458286!4458286 !25660055
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suck abstract from ncbi


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pmid25660055
      Eur+Heart+J 2015 ; 36 (22 ): 1405-14
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  • Expression of functional tissue factor by neutrophil extracellular traps in culprit artery of acute myocardial infarction #MMPMID25660055
  • Stakos DA ; Kambas K ; Konstantinidis T ; Mitroulis I ; Apostolidou E ; Arelaki S ; Tsironidou V ; Giatromanolaki A ; Skendros P ; Konstantinides S ; Ritis K
  • Eur Heart J 2015[Jun]; 36 (22 ): 1405-14 PMID25660055 show ga
  • AIMS: Neutrophil extracellular traps (NETs) are chromatin ?laments released by activated polymorphonuclear neutrophils (PMNs) and decorated with granule proteins with various properties. Several lines of evidence implicate NETs in thrombosis. The functional significance and the in vivo relevance of NETs during atherothrombosis in humans have not been addressed until now. METHODS AND RESULTS: Selective sampling of thrombotic material and surrounding blood from the infarct-related coronary artery (IRA) and the non-IRA was performed during primary percutaneous revascularization in 18 patients with ST-segment elevation acute myocardial infarction (STEMI). Thrombi isolated from IRA contained PMNs and NETs decorated with tissue factor (TF). Although TF was expressed intracellularly in circulating PMNs of STEMI patients, active TF was specifically exposed by NETs obtained from the site of plaque rupture. Treatment of NET structures with DNase I abolished TF functionality measurement. In vitro treatment of control PMNs with plasma obtained from IRA and non-IRA was further shown to induce intracellular up-regulation of TF but not NET formation. A second step consisting of the interaction between PMNs and thrombin-activated platelets was required for NET generation and subsequent TF exposure. CONCLUSION: The interaction of thrombin-activated platelets with PMNs at the site of plaque rupture during acute STEMI results in local NET formation and delivery of active TF. The notion that NETs represent a mechanism by which PMNs release thrombogenic signals during atherothrombosis may offer novel therapeutic targets.
  • |Analysis of Variance [MESH]
  • |Case-Control Studies [MESH]
  • |Coronary Thrombosis/metabolism/surgery [MESH]
  • |Coronary Vessels/*metabolism [MESH]
  • |Extracellular Traps/*metabolism [MESH]
  • |Female [MESH]
  • |Humans [MESH]
  • |Leukocytes, Mononuclear/physiology [MESH]
  • |Male [MESH]
  • |Middle Aged [MESH]
  • |Myocardial Infarction/*metabolism/surgery [MESH]
  • |Myocardial Revascularization/methods [MESH]
  • |Neutrophils/*metabolism [MESH]
  • |Percutaneous Coronary Intervention [MESH]
  • |Plaque, Atherosclerotic [MESH]
  • |Platelet Activation/physiology [MESH]
  • |Rupture, Spontaneous/metabolism [MESH]
  • |Thrombin/metabolism [MESH]


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