Neutrophil extracellular traps in ischemic stroke thrombi

  title={Neutrophil extracellular traps in ischemic stroke thrombi},
  author={Elodie Laridan and Frederik Denorme and Linda Desender and Olivier François and Tommy Andersson and H. Deckmyn and Karen Vanhoorelbeke and S. F. De Meyer},
  journal={Annals of Neurology},
Neutrophil extracellular traps (NETs) have been shown to promote thrombus formation. Little is known about the exact composition of thrombi that cause ischemic stroke. In particular, no information is yet available on the presence of NETs in cerebral occlusions. Such information is, however, essential to improve current thrombolytic therapy with tissue plasminogen activator (t‐PA). This study aimed at investigating the presence of neutrophils and more specifically NETs in ischemic stroke… 
Neutrophil Extracellular Traps in Arterial and Venous Thrombosis
&NA; Thrombotic complications are still a major health risk worldwide. Our view on the pathophysiology of thrombosis has significantly changed since the discovery of neutrophil extracellular traps
Neutrophil extracellular traps promote tPA-induced brain hemorrhage via cGAS in mice with stroke
Filtration of tissue plasminogen activator (tPA) in a murine stroke model results in increased neutrophil extracellular trap (NET) formation, which could improve the safety of tPA administration for stroke.
Neutrophil Extracellular Trap Targeting Protects Against Ischemic Damage After Fibrin-Rich Thrombotic Stroke Despite Non-Reperfusion
The data strongly support that the pharmacological modulation of NETs in the acute phase of stroke, could be a promising strategy to repair the brain damage in ischemic disease, independently of the type of thrombosis involved.
Neutrophil extracellular traps contribute to tissue plasminogen activator resistance in acute ischemic stroke
  • Shuoqi Zhang, Yuze Cao, Lihua Wang
  • Biology, Medicine
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 2021
Circulating neutrophil extracellular traps (NETs) resistant to t‐PA have not been studied completely although NETs in thrombi may contribute to tissue plasminogen activator (t‐PA) resistance. This
Thrombus Neutrophil Extracellular Traps Content Impair tPA-Induced Thrombolysis in Acute Ischemic Stroke
Thrombus NETs content may be responsible for reperfusion resistance, including mechanical or pharmacological approaches with intravenous tPA, irrespectively of their etiology.
Neutrophil Extracellular Traps in Atherosclerosis and Thrombosis.
Mechanisms of NET formation, evidence for their involvement in atherosclerosis and thrombosis, and potential therapeutic regimens specifically targeting NET components are summarized.
Impact of Neutrophil Extracellular Traps on Thrombosis Formation: New Findings and Future Perspective
The mechanisms of NETs formation in detail are summarized in detail; the research progress ofNETs in venous thrombosis, arterial thromBosis, acquired disease-associated throm bosis, sepsis coagulation disorder; as well as the strategies to target NETs in thROMbosis prevention and treatment are summarized.
Pharmacological Modulation of Neutrophil Extracellular Traps Reverses Thrombotic Stroke tPA (Tissue-Type Plasminogen Activator) Resistance.
Whether NET pharmacological modulation can reverse tPA resistance and the role of TLR4 (Toll-like receptor 4), previously related to NET formation, in thrombosis is studied to open new avenues for recanalization of platelet-rich thrombi after stroke.
Neutrophil extracellular traps induce a hypercoagulable state in glioma
This work investigated the presence and potential role of NETs in the hypercoagulable state in glioma patients and evaluated the interaction between NETs and endothelial cells (ECs) in gl ioma patients.


Neutrophil extracellular traps form predominantly during the organizing stage of human venous thromboembolism development
A growing health problem, venous thromboembolism (VTE), including pulmonary embolism and deep vein thrombosis (DVT), requires refined diagnostic and therapeutic approaches and neutrophil extracellular traps as an important scaffold supporting thrombus stability is recognized.
Neutrophil extracellular trap (NET) impact on deep vein thrombosis.
It is proposed that drugs that inhibit NET formation or facilitate NET degradation may prevent or treat DVT, and how NETs could influence thrombolysis is discussed.
Neutrophils, neutrophil extracellular traps and interleukin-17 associate with the organisation of thrombi in acute myocardial infarction.
A large burden of neutrophils, neutrophil extracellular traps and IL17A and -F are important constituents of fresh and lytic thrombus after acute myocardial infarction and the specific colocalisation of these indicates a role duringThrombus stabilisation and growth.
Extracellular DNA traps promote thrombosis
It is reported that NETs provide a heretofore unrecognized scaffold and stimulus for thrombus formation and may further explain the epidemiological association of infection with thrombosis.
Thrombosis: tangled up in NETs.
The biological process of NET formation and how the extracellular release of DNA and protein components of NETs, such as histones and serine proteases, contributes to coagulation and platelet aggregation are described.
ADAMTS13-mediated thrombolysis of t-PA-resistant occlusions in ischemic stroke in mice.
Data show for the first time a potent thrombolytic activity of ADAMTS13 in the setting of stroke, which might become useful in treatment of acute ischemic stroke.
Tissue factor-positive neutrophils bind to injured endothelial wall and initiate thrombus formation.
The results show that the interaction of neutrophils with endothelial cells is a critical step preceding platelet accumulation for initiating arterial thrombosis in injured vessels and targeting neutrophil interacting with endothelium may constitute an efficient strategy to reduce thromBosis.
Coronary neutrophil extracellular trap burden and deoxyribonuclease activity in ST-elevation acute coronary syndrome are predictors of ST-segment resolution and infarct size.
PMNs are highly activated in ST-elevation acute coronary syndrome and undergo NETosis at the CLS, andCoronary NET burden and deoxyribonuclease activity are predictors of ST-segment resolution and myocardial infarct size.
Abundant neutrophil extracellular traps in thrombus of patient with microscopic polyangiitis
The collective findings suggest the possibility that thrombosis could be critically associated with MPA via NETs, and that NETs could be a therapeutic target in MPA patients.