Increased monocyte tissue factor expression in coronary disease.

Leatham, E; Bath, Philip M.W.; Tooze, J. Adam; Camm, A. John

doi:10.1136/hrt.73.1.10

Cited by 137 publications

(73 citation statements)

References 22 publications

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“…Thus, SAA could contribute to a hypercoagulable state, particularly if free to HDL-bound SAA levels were elevated. Studies also show increased basal TF levels in patients with cardiovascular disease (21), and, as SAA levels are also elevated in these patients (61), we propose that SAA, as a potent and rapid inducer of TF, may be a new link between inflammation and thrombosis. Importantly, blood-borne TF, in the form of microparticles, may contribute to thrombus formation and to vessel damage (62), although the factors that induce TF in the circulation of patients with inflammatory diseases are unclear.…”

Section: Discussionmentioning

confidence: 62%

“…Lymphocytes, which do not express TF themselves, are required for optimal TF production by monocytes/macrophages (18). Hypercoagulability associated with vascular disease is considered to be principally mediated by TF expressed within atherosclerotic plaque, and on monocytes in the circulation (20,21), and TF expression is associated with macrophage-mediated fibrin deposition, which is common in most inflammatory lesions (22). In this study, we show a potent and rapid induction of TF activity, mRNA, and protein on normal human monocytes by SAA.…”

Section: Serum Amyloid a Induces Monocyte Tissue Factormentioning

confidence: 99%

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Serum Amyloid A Induces Monocyte Tissue Factor

Cai

Song

Endoh

et al. 2007

The Journal of Immunology

107

121

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C-reactive protein (CRP) and serum amyloid A (SAA) increase in the blood of patients with inflammatory conditions and CRP-induced monocyte tissue factor (TF) may contribute to inflammation-associated thrombosis. This study demonstrates that SAA is a potent and rapid inducer of human monocyte TF. SAA induced TF mRNA in PBMC within 30 min and optimal procoagulant activity within 4 h, whereas CRP (25 μg/ml)-induced activity was minimal at this time. Unlike CRP, SAA did not synergize with LPS. Procoagulant activity was inhibited by anti-TF and was dependent on factors VII and X, and TF Ag levels were elevated on CD14+ monocytes. Responses were optimal with lymphocytes, although these were not obligatory. Inhibitor studies indicate activation of NF-κB through the ERK1/2 and p38 MAPK pathways; the cyclo-oxygenase pathway was not involved. SAA-induced TF was partially inhibited by high-density lipoprotein, but not by low-density lipoprotein or by apolipoprotein A-I. SAA is a ligand for the receptor for advanced glycation end products (RAGE), and TF generation was suppressed by ∼50% by a RAGE competitor, soluble RAGE, and by ∼85% by anti-RAGE IgG. However, another RAGE ligand, high mobility group box-1 protein, capable of inducing monocyte chemotactic protein-1 mRNA in 2 h, did not induce TF within 24 h. Cross-linking studies confirmed SAA binding to soluble RAGE. Elevated SAA is a marker of disease activity in patients with rheumatoid arthritis, and PBMC from patients with rheumatoid arthritis were more sensitive to SAA than normals, suggesting a new link between inflammation and thrombosis.

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Section: Discussionmentioning

confidence: 62%

Section: Serum Amyloid a Induces Monocyte Tissue Factormentioning

confidence: 99%

Serum Amyloid A Induces Monocyte Tissue Factor

Cai

Song

Endoh

et al. 2007

The Journal of Immunology

107

121

View full text Add to dashboard Cite

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“…6,7) Furthermore, monocytes isolated from UA patients were shown to be in an activated state with respect to the expression of a tissue factor (TF) which has a pro-coagulating activity. 8,9) T-lymphocytes expressing activation markers such as very late activation antigen-1 (VLA-1) and HLA-DR have been reportedly found in atherosclerotic plaques. 10) These T-lymphocytes release cytokines such as interferon (IFN)-γ which causes the plaques to become unstable.…”

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confidence: 99%

Correlation between Monocyte and T-lymphocyte Activation Markers in Patients with Acute Coronary Syndrome.

Choi

Lee

et al. 2000

Jpn Heart J

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SUMMARYEvidence suggesting the involvement of activated monocytes and T-lymphocytes in the acute phase of coronary artery disease (CAD) has been increasing. But a detailed analysis of a correlation between monocyte and T-lymphocyte activation markers in CAD has not yet been done. We analyzed plasma C-reactive protein (CRP) levels and the expression levels of CD14 and CD11b on monocytes and the percentage of HLA-DR + T-lymphocytes in 25 patients with acute coronary syndrome (ACS), 12 stable angina (SA) patients, and 23 control subjects using flow-cytometry. The expression of CD14 by monocytes was increased significantly in ACS patients (activation index = 38.7 ± 2.5, mean ± SEM) in comparison to the control subjects (8.0 ± 1.9) and the SA patients (16.9 ± 3.9) (p < 0.001 and p < 0.01, respectively). The expression of CD11b by monocytes of ACS patients (4.6 ± 0.6) was also increased significantly in comparison to control subjects (2.2 ± 0.1) and the SA patients (2.2 ± 0.3) (p < 0.001 for both). Also, a significantly higher percentage of HLA-DR positive T-lymphocytes (19.2 ± 1.8 vs 13.5 ± 1.2%, p < 0.05) was observed among ACS patients in comparison to control subjects. Significant increases in plasma CRP levels were also detected in ACS patients. Furthermore, there were statistically significant correlations among these activation markers. These results indicate that activation of inflammatory cells may play a role in the pathogenesis of ACS. The correlation between the activation status of monocytes and T-lymphocytes indicates that the activation of these immune cells is linked in such a way that activation of one type of cell may lead to the activation of another type of cell. (Jpn Heart J 2000; 41: 605-615) Key words: CD14, CD11b, HLA-DR, Unstable angina, Stable angina, Inflammation, Flow cytometry INCREASING evidence suggests that inflammatory changes and activation of immune cells are involved in the acute phase of atherosclerosis.1) The atherosclerotic plaques of AMI and UA patients are considered active plaques and vulneraFrom the Cardiology Division, Cardiovascular Institute,

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“…11) Plasma levels of TF and tissue factor pathway inhibitor (TFPI), which regulates the initial step of the extrinsic coagulation pathway mediated by TF, are increased in myocardial infarction and unstable angina. [12][13][14] Plasminogen activator inhibitor type-1 (PAI-1), a physiologic inhibitor of plasminogen activators, plays a crucial role in modulating intravascular thrombosis and thrombolysis, 15) and hypofibrinolysis is associated with the risk of accelerated atherosclerosis. 16) Thus, the correlation between atherogenic cytokines and hemostatic parameters with early atherosclerotic functional changes of brachial artery FMD and morphological changes of intima-media thickness (IMT) in the common carotid arteries was investigated.…”

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confidence: 99%

Relationships between Brachial Artery Flow Mediated Dilation and Carotid Artery Intima-Media Thickness in Patients with Suspected Coronary Artery Disease.

et al. 2002

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SUMMARYThe correlation of peripheral endothelial dysfunction and intima-media thickness (IMT) in patients with suspected coronary artery disease (CAD) has been unclear. Inflammation and thrombosis may play a role at early stages of atherosclerosis. Thus, early atherosclerosis was noninvasively examined morphologically by IMT of carotid arteries, and functionally by flow mediated dilation (FMD) of brachial arteries in patients who were suspected of CAD and had undergone coronary angiography. Plasma antigen levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6, representative atherogenic cytokines, tissue factor (TF) and tissue factor pathway inhibitor (TFPI), markers of coagulation, and plasma activity level of plasminogen activator inhibitor type-1 (PAI-1), a marker of defective fibrinolysis, were measured. Patients with coronary atherosclerosis in one or more vessels with lesion ≥50% had significantly reduced FMD compared with those with angiographically normal coronary arteries. Carotid artery IMT increased significantly only in patients with advanced coronary atherosclerosis in one or more vessels with lesion ≥90%. Plasma antigen levels of IL-6 were significantly increased in patients with reduced FMD (<5%) compared to those in patients with FMD between 10 and 15%. Plasma antigen levels of TF, total and free TFPI, and PAI-1 activity tended to increase with a reduction in FMD. Thus, (1) FMD was reduced at early stages of CAD while IMT was increased in advanced CAD, and (2) inflammation and thrombosis may play a role in the early stages of the atherosclerotic process. (Jpn Heart J 2002; 43: 117-125)

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Increased monocyte tissue factor expression in coronary disease.

Abstract: Objective-To investigate whether monocyte expression of tissue factor is increased in patients with acute coronary syndromes and chronic stable angina.

Cited by 137 publications

References 22 publications

Serum Amyloid A Induces Monocyte Tissue Factor

Serum Amyloid A Induces Monocyte Tissue Factor

Correlation between Monocyte and T-lymphocyte Activation Markers in Patients with Acute Coronary Syndrome.

Relationships between Brachial Artery Flow Mediated Dilation and Carotid Artery Intima-Media Thickness in Patients with Suspected Coronary Artery Disease.

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