Plasma TF activity predicts cardiovascular mortality in patients with acute myocardial infarction

Steppich, Birgit; Braun, Siegmund; Stein, Andreas; Demetz, Gabriele; Groha, Philipp; Schömig, Albert; Beckerath, Nicolas von; Kastrati, Adnan; Ott, Ilka

doi:10.1186/1477-9560-7-11

Cited by 39 publications

(30 citation statements)

References 35 publications

(29 reference statements)

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“…Encryption/decryption appears primarily to be a function of membrane microenvironment. When TF is present on the plasma membrane in an encrypted form it can still bind FVII but only acts as a cytokine receptor capable of transmitting intracellular signals and cannot activate Factor X [50-52]. Decryption leads to activation of the ability to cleave Factor X and subsequent procoagulant activity, and occurs after cell exposure to various agents [53-55].…”

Section: Regulation Of Tf Expression and Activitymentioning

confidence: 99%

“…For example, TF activity increases after cell exposure to freeze-thaw cycles, calcium ionophore and phorbol myristate acetate (PMA) [56,57], stimuli that do not alter TF transcription or translation. Other factors shown to be involved in encryption/decryption include nonionic detergents, apoptosis, phosphatidyl serine exposure, lipid raft dissociation and disulfide linkage of Cysteine 186-Cysteine 209 [52,56,58,59]. Thus, regulation of gene expression, post-translational modifications and factors that regulate TF enzymatic activity may all be important in modulating TF activity in the lung.…”

Section: Regulation Of Tf Expression and Activitymentioning

confidence: 99%

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Therapeutic Modulation of Coagulation and Fibrinolysis in Acute Lung Injury and the Acute Respiratory Distress Syndrome

Sebag¹,

Bastarache²,

Ware³

2011

CPB

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Acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) are characterized by excessive intra-alveolar fibrin deposition, driven, at least in part by inflammation. The imbalance between activation of coagulation and inhibition of fibrinolysis in patients with ALI/ARDS favors fibrin formation and appears to occur both systemically and in the lung and airspace. Tissue factor (TF), a key mediator of the activation of coagulation in the lung, has been implicated in the pathogenesis of ALI/ARDS. As such, there have been numerous investigations modulating TF activity in a variety of experimental systems in order to develop new therapeutic strategies for ALI/ARDS. This review will summarize current understanding of the role of TF and other proteins of the coagulation cascade as well the fibrinolysis pathway in the development of ALI/ARDS with an emphasis on the pathways that are potential therapeutic targets. These include the TF inhibitor pathway, the protein C pathway, antithrombin, heparin, and modulation of fibrinolysis through plasminogen activator-1 (PAI-1) or plasminogen activators (PA). Although experimental studies show promising results, clinical trials to date have proven unsuccessful in improving patient outcomes. Modulation of coagulation and fibrinolysis has complex effects on both hemostasis and inflammatory pathways and further studies are needed to develop new treatment strategies for patients with ALI/ARDS.

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Section: Regulation Of Tf Expression and Activitymentioning

confidence: 99%

Section: Regulation Of Tf Expression and Activitymentioning

confidence: 99%

Therapeutic Modulation of Coagulation and Fibrinolysis in Acute Lung Injury and the Acute Respiratory Distress Syndrome

Sebag¹,

Bastarache²,

Ware³

2011

CPB

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“…Therefore quantitative circulating MV measurement in cardiovascular patients has been proposed as a way to generate diagnostic and prognostic information [18][19][20][21][22].…”

Section: Introductionmentioning

confidence: 99%

Dynamic microvesicle release and clearance within the cardiovascular system: triggers and mechanisms

et al. 2015

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Interest in cell-derived microvesicles (or microparticles) within cardiovascular diagnostics and therapeutics is rapidly growing. Microvesicles are often measured in the circulation at a single time point. However, it is becoming clear that microvesicle levels both increase and decrease rapidly in response to certain stimuli such as hypoxia, acute cardiac stress, shear stress, hypertriglyceridaemia and inflammation. Consequently, the levels of circulating microvesicles will reflect the balance between dynamic mechanisms for release and clearance. The present review describes the range of triggers currently known to lead to microvesicle release from different cellular origins into the circulation. Specifically, the published data are used to summarize the dynamic impact of these triggers on the degree and rate of microvesicle release. Secondly, a summary of the current understanding of microvesicle clearance via different cellular systems, including the endothelial cell and macrophage, is presented, based on reported studies of clearance in experimental models and clinical scenarios, such as transfusion or cardiac stress. Together, this information can be used to provide insights into potential underlying biological mechanisms that might explain the increases or decreases in circulating microvesicle levels that have been reported and help to design future clinical studies.

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“…Other studies have also shown that the TF +5466 A/G polymorphism modulates thrombin generation initiated by vascular injury. However, other studies show no relationship between the expression of TF and increased risk of thrombus formation (Davis and Erlich, 2008;Steppich et al, 2009;Zhou et al, 2011).…”

Section: Discussionmentioning

confidence: 93%

Lack of association between potential prothrombotic genetic risk factors and arterial and venous thrombosis

Evangelista¹,

Rios²,

Ribeiro³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Recent studies have shown an association between thrombosis and factor VII (FVII), tissue factor (TF), and angiotensinconverting enzyme (ACE). This suggests that individuals with FVII-402 G/A, FVII-401 G/T, TF+5466 A/G, and ACE-287 insertion/ deletion (I/D) polymorphisms present an increased risk of venous thrombosis, heart disease, and ischemic stroke compared with controls. In this study, we investigated the frequencies of these polymorphisms and their association with arterial and venous thrombosis. For the FVII-402 G/A polymorphism, there were 57.3% heterozygote (HT) genotypes and 8.3% homozygote (HM) genotypes in the patients, and 45.2% HT genotypes and 15.4% HM genotypes in the controls. For the FVII-401 G/T polymorphism, there were 37.5% HT genotypes and 3.1% HM genotypes in the patients, and 32.7% HT genotypes and 4.8% HM genotypes in the controls. The polymorphism TF+5466 A/G was not found in any of the samples analyzed. For the ACE-287 I/D polymorphism, there were 43 (40.6%) HT genotypes and 63 (59.4%) HM genotypes in the controls and 28 (45.2%) HT genotypes and 34 (54.8%) HM genotypes in the patients. No significant difference was observed by comparing patients and controls. In this study, no association was found between the presence of the evaluated polymorphisms and the occurrence of thrombotic events.

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Plasma TF activity predicts cardiovascular mortality in patients with acute myocardial infarction

Cited by 39 publications

References 35 publications

Therapeutic Modulation of Coagulation and Fibrinolysis in Acute Lung Injury and the Acute Respiratory Distress Syndrome

Therapeutic Modulation of Coagulation and Fibrinolysis in Acute Lung Injury and the Acute Respiratory Distress Syndrome

Dynamic microvesicle release and clearance within the cardiovascular system: triggers and mechanisms

Lack of association between potential prothrombotic genetic risk factors and arterial and venous thrombosis

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