Assessment of plasma tissue factor activity in patients presenting with coronary artery disease: limitations of a commercial assay

Bogdanov, Vladimir Y.; Cimmino, Giovanni; Tardos, Jonathan G.; Tunstead, James; Badimón, Juan J.

doi:10.1111/j.1538-7836.2009.03315.x

Cited by 35 publications

(32 citation statements)

References 9 publications

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“…We have reported that in another subset of CAD patients, there is a decrease in plasma TF activity [49]. Taken together, our study reinforces the notion that potentially active TF is always present in plasma.…”

Section: Is Blood-borne Tf Active?supporting

confidence: 89%

“…Despite the predictive role of plasma TF antigen in patients with coronary artery disease (CAD) reported by different groups [45,46], conflicting observations have been also reported [47,48]; in some cases, such as the FRISC II study group, despite significant high levels of TF antigen in CAD patients compared to control group, these heightened levels are not predictive of the clinical outcome [47]. Data from our laboratory indicate that in CAD plasma, circulating MP do not carry all functional TF, yet, they strongly potentiate FXa generation in a TF-and FVIIa-independent manner [49].…”

Section: Is Blood-borne Tf Active?contrasting

confidence: 57%

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Pathophysiological role of blood-borne tissue factor: should the old paradigm be revisited?

Cimmino

Golino

Badimón³

2010

Intern Emerg Med

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The term "vulnerable plaque" identifies atherosclerotic lesions prone to rupture. Plaque disruption facilitates the interaction of the inner components of the lesion, tissue factor (TF) among them, with the flowing blood. This results in activation of the coagulation cascade, ultimately leading to thrombus formation, and abrupt vascular occlusion. Despite the central role of vulnerable plaques in the onset of acute coronary syndromes (ACS), there are certain conditions (e.g., eroded plaques) where a hyperactive, "vulnerable" blood, may play a predominant pathophysiological role. Recently, two distinct pools of circulating TF have been identified. One, associated with cell-derived microparticles probably originating from apoptotic cells, such as macrophages, smooth muscle cells, and endothelium. The most recent, blood-borne TF, circulates in an "inactive" form (encryption) and has to be activated (decryption) to exert its thrombogenic activity. Certain pathological conditions associated with an increased rate of thrombotic complications have been associated with high levels of circulating TF. It is thought that the blood-borne TF perpetuates the initial thrombogenic stimulus, leading to the formation of larger or more stable thrombus, and thus, more severe ACS. Thus, the concept of vulnerable blood could represent a new link between the vulnerable lesion and the high-risk patient. Therefore, the assessment of selected biomarkers associated with "vulnerable or hyperreactive blood", e.g., blood-borne tissue factor, may represent a useful tool to identify patients with a high-risk profile of developing major cardiovascular events.

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Section: Is Blood-borne Tf Active?supporting

confidence: 89%

Section: Is Blood-borne Tf Active?contrasting

confidence: 57%

Pathophysiological role of blood-borne tissue factor: should the old paradigm be revisited?

Cimmino

Golino

Badimón³

2010

Intern Emerg Med

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“…In fact, the relative expression of fl-TF and asTF is in favor of fl-TF in human atherosclerotic plaques and it remains undetermined how much asTF is expressed in vivo. Moreover, in our studies we used re-lipidated fl-TF to mimic the effect of circulating fl-TF 42, 43 , an approach that does not reflect the proteome complexity of circulating microparticles carrying fl-TF in humans.…”

Section: Discussionmentioning

confidence: 99%

Alternatively Spliced Tissue Factor Promotes Plaque Angiogenesis Through the Activation of Hypoxia-Inducible Factor-1α and Vascular Endothelial Growth Factor Signaling

Giannarelli¹,

Alique²,

Rodriguez³

et al. 2014

Circulation

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Background Alternatively Spliced Tissue Factor (asTF) is a novel isoform of full-length Tissue Factor (fl-TF) that exhibits angiogenic activity. Although asTF has been detected in human plaques, it is unknown whether its expression in atherosclerosis causes increased neovascularization and an advanced plaque phenotype. Methods and Results Carotid (n=10) and coronary specimens (n=8), from patients with stable or unstable angina, were classified as complicated or uncomplicated based on plaque morphology. Analysis of asTF expression and cell type –specific expression revealed a strong expression and co-localization of asTF with macrophages and neovessels within complicated, but not un-complicated, human plaques. Our results showed that the angiogenic activity of asTF is mediated via HIF-1α up-regulation through integrins and activation of phosphatidylinositol-kinase (PI3K)/Akt and mitogen-activated protein kinase (MAPK) pathways. HIF-1α up-regulation by asTF also was associated with increased VEGF expression in primary human endothelial cells, and VEGF-Trap significantly reduced the angiogenic effect of asTF in vivo. Furthermore, asTF gene transfer significantly increased neointima formation and neovascularization following carotid wire injury in ApoE−/− mice. Conclusions The results of this study provide strong evidence that asTF promotes neointima formation and angiogenesis in an experimental model of accelerated atherosclerosis. Herein, we demonstrate that the angiogenic effect of asTF is mediated via the activation of the HIF-1/VEGF signaling. This mechanism may be relevant to neovascularization, progression and associated complications of human atherosclerosis as suggested by the increased expression of asTF in complicated vs. uncomplicated human carotid and coronary plaques.

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“…Alternatively, Khan et al suggested that soluble TF can bind to peripheral monocytes and platelets and efficiently activate factor VII [133]. The potential origin of this discrepancy could be assigned to the physiologically irrelevant conditions [3, 124] used and the lack of validated commercial assays for the detection of alternatively spliced TF activity at its physiologic concentrations [134–136]. TF antigen in blood may also be detected as a degradation product and not necessarily as an alternatively spliced form.…”

Section: Presentationmentioning

confidence: 99%

Tissue Factor Structure and Function

Butenas

2012

Scientifica

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Tissue factor (TF) is an integral membrane protein that is essential to life. It is a component of the factor VIIa-TF complex enzyme and plays a primary role in both normal hemostasis and thrombosis. With a vascular injury, TF becomes exposed to blood and binds plasma factor VIIa, and the resulting complex initiates a series of enzymatic reactions leading to clot formation and vascular sealing. Many cells, both healthy, and tumor cells, produce detectable amounts of TF, especially when they are stimulated by various agents. Despite the relative simplicity and small size of TF, there are numerous contradictory reports about the synthesis and presentation of TF on blood cells and circulation in normal blood either on microparticles or as a soluble protein. Another subject of controversy is related to the structure/function of TF. It has been almost commonly accepted that cell-surface-associated TF has low (if any) activity, that is, is “encrypted” and requires specific conditions/reagents to become active, that is, “decrypted.” However there is a lack of agreement related to the mechanism and processes leading to alterations in TF function. In this paper TF structure, presentation, and function, and controversies concerning these features are discussed.

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Assessment of plasma tissue factor activity in patients presenting with coronary artery disease: limitations of a commercial assay

Cited by 35 publications

References 9 publications

Pathophysiological role of blood-borne tissue factor: should the old paradigm be revisited?

Pathophysiological role of blood-borne tissue factor: should the old paradigm be revisited?

Alternatively Spliced Tissue Factor Promotes Plaque Angiogenesis Through the Activation of Hypoxia-Inducible Factor-1α and Vascular Endothelial Growth Factor Signaling

Tissue Factor Structure and Function

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