Tissue factor as an effector of angiogenesis and tumor progression in hematological malignancies

López‐Pedrera, Chary; Barbarroja, Nuria; Dorado, Gabriel; Siendones, Emilio; Velasco, Francisco

doi:10.1038/sj.leu.2404264

Cited by 68 publications

(55 citation statements)

References 88 publications

(79 reference statements)

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“…There is accumulating experimental evidence for a role of fibrin and fibrinogen degradation products in carcinogenesis by promoting invasive growth, angiogenesis, and metastasis. 36,71,72 ITGB3 codes for the beta subunit of the glycoprotein IIb/IIIa complex, which mediates platelet aggregation by serving as a receptor for fibrinogen. The ITGB3 For personal use only.…”

Section: Discussionmentioning

confidence: 99%

Genetic variation in 1253 immune and inflammation genes and risk of non-Hodgkin lymphoma

Cerhan¹,

Ansell²,

Fredericksen³

et al. 2007

Blood

146

145

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Smaller-scale evaluations suggest that common genetic variation in candidate genes related to immune function may predispose to the development of non-Hodgkin lymphoma (NHL). We report an analysis of variants within genes associated with immunity and inflammation and risk of NHL using a panel of 9412 single-nucleotide polymorphisms (SNPs) from 1253 genes in a study of 458 patients with NHL and 484 frequencymatched controls. We modeled haplotypes and risk of NHL, as well as the main effects for all independent SNPs from a gene in multivariate logistic regression models; we separately report results for nonsynonymous (ns) SNPs. In gene-level analyses, the strongest findings (P < .001) were for CREB1, FGG, MAP3K5, RIPK3, LSP1, TRAF1, DUSP2, and ITGB3. In nsSNP analyses, the strongest findings (P < .01) were for ITGB3 L59P (odds ratio [

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Section: Discussionmentioning

confidence: 99%

Genetic variation in 1253 immune and inflammation genes and risk of non-Hodgkin lymphoma

Cerhan¹,

Ansell²,

Fredericksen³

et al. 2007

Blood

146

145

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“…One of these proteins is tissue factor (TF). [7][8][9] TF is the cellular receptor and cofactor for blood coagulation factor VII (FVII). 10,11 In addition to its primary role in blood coagulation, accumulating evidence has transformed our view of TF from the cellular receptor for activated FVII (FVIIa) to a multifaceted transmembrane signaling receptor.…”

Section: See Accompanying Article On Page 2364mentioning

confidence: 99%

Tissue Factor Regulates Microvessel Formation and Stabilization by Induction of Chemokine (C-C motif) Ligand 2 Expression

Arderiu

Peña

Aledo

et al. 2011

ATVB

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Objective-Tissue factor (TF) triggers arterial thrombosis. TF is also able to initiate cellular signaling mechanisms leading to angiogenesis. Because high cardiovascular risk atherosclerotic plaques show significant angiogenesis, our objective was to investigate whether TF is able to trigger and stabilize atherosclerotic plaque neovessel formation. Methods and Results-In this study, we showed, by real-time confocal microscopy in 3-dimensional basement membrane cocultures, that TF in human microvascular endothelial cells (HMEC-1) and in human vascular smooth muscle cells (HVSMCs) plays an important role in the formation of capillary-like networks. TF silencing in endothelial cells and smooth muscle cells inhibits the formation of tube-like structures with stable phenotype. Using an in vivo model, we observed that TF inhibition in either HMEC-1 or HVSMCs reduced their shared ability to form new capillaries. The phenotypic changes induced by TF silencing were linked to reduced chemokine (C-C motif) ligand 2 (CCL2) expression in endothelial cells. Wound healing and chemotactic assays demonstrated that TF-induced release of CCL2 stimulated HVSMC migration to HMEC-1. Key Words: angiogenesis Ⅲ atherosclerosis Ⅲ cytokines Ⅲ endothelial function Ⅲ vascular biology A therosclerotic plaque angiogenesis, the outgrowth of new capillaries from preexisting vascular networks, is a pathological feature of advanced complicated plaques. 1,2 Interestingly, coronary type VI plaques, according to the American Heart Association classification, are those with higher amount of microvessels and those with higher risk of inducing a clinical cardiovascular event. 3 In advanced plaques, inflammatory cell infiltration and concomitant production of proangiogenic cytokines may be responsible for induction of uncontrolled neointimal microvessel proliferation resulting in production of immature and fragile neovessels. The final stage of microvessel formation occurs when maturation requires the formation of tight endothelial cell-tocell contacts, 4 the downregulation of endothelial proliferation, and the deposition of a basal lamina to which the endothelium tightly adheres, as well as the recruitment of supporting cells to the vessel wall, such as pericytes and smooth muscle cells (SMCs). 5,6 During angiogenesis, the communication between endothelial cells (ECs) and SMCs requires a precise temporal and spatial regulation of pro-and antiangiogenic molecules, but the process is not yet fully understood. Conclusion-Endogenous See accompanying article on page 2364In recent years, it has become clear that the angiogenesis process is highly dependent on components of the blood coagulation cascade. One of these proteins is tissue factor (TF). 7-9 TF is the cellular receptor and cofactor for blood coagulation factor VII (FVII). 10,11 In addition to its primary role in blood coagulation, accumulating evidence has transformed our view of TF from the cellular receptor for activated FVII (FVIIa) to a multifaceted transmembrane signaling receptor. The bioch...

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“…Monocytes and macrophages are known to express TF upon stimulation by inflammation-related agents (Nijziel et al , 2001 ;Broussas et al , 2002 ;Levi et al , 2006 ). In addition to normal tissues and cells, TF is also known to be expressed by tumor cells, where it is related to the metastatic potential of those cells (Edwards et al , 1981 ;Lopez -Pedrera et al, 2006 ). Furthermore, a role for TF in the progression of cardiovascular disease has been suggested (Mumford and McVey , 2004 ;Jude et al , 2005 ).…”

Section: Introductionmentioning

confidence: 99%

Comparison of natural and recombinant tissue factor proteins: new insights

Butenas

2013

Biological Chemistry

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Tissue factor (TF), an initiator of blood coagulation in vivo , is expressed in a variety of cells. Sufficient natural TF has been isolated to clone and express recombinant proteins ranging from full-length TF to its extracellular domain. Because of the limited availability of natural TF, recombinant proteins have been used as surrogates. Despite the differences in their post-translational modifications, it has been accepted that membrane-anchored recombinant TFs are quite similar to the natural TF. Recent studies, however, have shown that post-translational modifications play an important role in TF-triggered thrombin generation.

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Tissue factor as an effector of angiogenesis and tumor progression in hematological malignancies

Cited by 68 publications

References 88 publications

Genetic variation in 1253 immune and inflammation genes and risk of non-Hodgkin lymphoma

Genetic variation in 1253 immune and inflammation genes and risk of non-Hodgkin lymphoma

Tissue Factor Regulates Microvessel Formation and Stabilization by Induction of Chemokine (C-C motif) Ligand 2 Expression

Comparison of natural and recombinant tissue factor proteins: new insights

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