Histamine differentially interacts with tumor necrosis factor‐α and thrombin in endothelial tissue factor induction: the role of c‐Jun NH2‐terminal kinase

Steffel, Jan; Arnet, Claudine; Akhmedov, Alexander; Iseli, Sarah; Lüscher, Thomas F.; Tanner, Felix C.

doi:10.1111/j.1538-7836.2006.02175.x

Cited by 13 publications

(12 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous reports have shown that TNF-a enhances induction of TF by histamine and thrombin in a concentration-dependent manner, and was amplified by paclitaxel. 22 Other reports also showed that expression of TNF-a receptor-1 in arterial walls accelerate atherosclerotic lesions. 8 The coagulation cascade results in the deposition of fibrin, which is cleared by tissue plasminogen activator released from endothelial cells.…”

Section: Discussionmentioning

confidence: 97%

Paclitaxel Potentiates Inflammatory Cytokine-induced Prothrombotic Molecules in Endothelial Cells

Wood¹,

Xing²,

Tesfamariam³

2010

Journal of Cardiovascular Pharmacology

View full text Add to dashboard Cite

To overcome the limitations of balloon expandible metal stent-induced neointimal smooth muscle cell proliferation, drug-coated stent devices have been developed. Drug eluting stents release high concentrations of antiproliferative agents, such as paclitaxel, to reduce neointimal hyperplasia. The proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), is known to cause severe endothelial dysfunction and accelerate atherosclerotic lesion progression. The interaction of TNF-alpha and paclitaxel on the release of prothrombotic molecules was examined in endothelial cells. Treatment of endothelial cells with paclitaxel had no direct effect on tissue factor (TF) expression, but TNF-alpha increased TF. Cotreatment of paclitaxel with TNF-alpha markedly augmented the release of TF. TNF-alpha induced release of plasminogen activator inhibitor but no synergism occurred with paclitaxel. Treatment of endothelial cells with paclitaxel and TNF-alpha reduced expression of thrombomodulin and protein C receptor. Tissue factor pathway inhibitor expression was reduced by prolonged treatment with either paclitaxel or TNF-alpha. The adhesion molecule, CD62 E, was induced by TNF-alpha; however, CD31, CD62 P, and CD106 were not affected by paclitaxel and TNF-alpha. Apoptosis was not observed with cotreatment of endothelial cells with paclitaxel and TNF-alpha. CD59-positive microparticles were released in response to TNF-alpha, but the release was not augmented by paclitaxel. Paclitaxel and TNF-alpha increased the nitrotyrosination of proteins. These findings indicate that paclitaxel enhances TNF-alpha-induced release of TF, and downregulated thrombomodulin, increased protein nitration, which may subsequently favor prothrombotic intimal surface.

show abstract

Section: Discussionmentioning

confidence: 97%

Paclitaxel Potentiates Inflammatory Cytokine-induced Prothrombotic Molecules in Endothelial Cells

Wood¹,

Xing²,

Tesfamariam³

2010

Journal of Cardiovascular Pharmacology

View full text Add to dashboard Cite

show abstract

“…Histamine-induced vascular contractions, 11,17 as well as expression of tissue factor 12,13 , a key trigger of the coagulation cascade, are mediated via this receptor. In line with these findings, the present data indicate that activation of the H1 receptor, but not the H2 receptor, promotes the formation of atherosclerotic lesions.…”

Section: Discussionmentioning

confidence: 99%

Histamine H1 Receptor Promotes Atherosclerotic Lesion Formation by Increasing Vascular Permeability for Low-Density Lipoproteins

Rozenberg

Sluka

Rohrer

et al. 2010

ATVB

View full text Add to dashboard Cite

Objective-Enhanced endothelial permeability leading to intimal accumulation of low-density lipoproteins (LDL) stimulates the formation of atherosclerotic lesions. Histamine is known to increase vascular permeability. Whether this affects the formation of atherosclerotic lesions, however, remains elusive. Methods and Results-Apolipoprotein E-null (ApoE Ϫ/Ϫ ) mice treated with a histamine H1 receptor but not an H2 receptor antagonist developed 40% fewer atherosclerotic lesions in the aorta than placebo-treated controls. Similarly, genetic deletion of the H1 but not the H2 receptor resulted in a 60% reduction of lesions compared with ApoE Ϫ/Ϫ controls. The H1 receptor enhanced LDL permeability and lipid accumulation in the aorta, whereas plasma lipoprotein levels remained unaltered. In contrast, the H1 receptor did not affect proliferation and migration of vascular smooth muscle cells. Bone marrow transplantation confirmed that the formation of atherosclerotic lesions depended on the H1 receptor in vascular cells, whereas its presence in bone marrow-derived cells was irrelevant for plaque development. Mice expressing the H1 receptor exhibited higher levels of the chemokine (C-C motif) ligand 5 and higher numbers of macrophages and T-helper lymphocytes in plaques, higher numbers of circulating lymphocytes, and larger spleens.

show abstract

“…Histamine has been shown to induce the expression of TF in vascular cells activating the H1, but not the H2, receptor (59, 60), revealing the potential effect of histamine on the extrinsic coagulation pathway. Some newly generated cytokines from mast cells, such as IL-6, also affect the coagulation system.…”

Section: The Coagulation System In Anaphylaxismentioning

confidence: 99%

The Mast Cell, Contact, and Coagulation System Connection in Anaphylaxis

et al. 2017

View full text Add to dashboard Cite

Anaphylaxis is the most severe form of allergic reaction, resulting from the effect of mediators and chemotactic substances released by activated cells. Mast cells and basophils are considered key players in IgE-mediated human anaphylaxis. Beyond IgE-mediated activation of mast cells/basophils, further mechanisms are involved in the occurrence of anaphylaxis. New insights into the potential relevance of pathways other than mast cell and basophil degranulation have been unraveled, such as the activation of the contact and the coagulation systems. Mast cell heparin released upon activation provides negatively charged surfaces for factor XII (FXII) binding and auto-activation. Activated FXII, the initiating serine protease in both the contact and the intrinsic coagulation system, activates factor XI and prekallikrein, respectively. FXII-mediated bradykinin (BK) formation has been proven in the human plasma of anaphylactic patients as well as in experimental models of anaphylaxis. Moreover, the severity of anaphylaxis is correlated with the increase in plasma heparin, BK formation and the intensity of contact system activation. FXII also activates plasminogen in the fibrinolysis system. Mast cell tryptase has been shown to participate in fibrinolysis through plasmin activation and by facilitating the degradation of fibrinogen. Some usual clinical manifestations in anaphylaxis, such as angioedema or hypotension, or other less common, such as metrorrhagia, may be explained by the direct effect of the activation of the coagulation and contact system driven by mast cell mediators.

show abstract

Histamine differentially interacts with tumor necrosis factor‐α and thrombin in endothelial tissue factor induction: the role of c‐Jun NH2‐terminal kinase

Cited by 13 publications

References 43 publications

Paclitaxel Potentiates Inflammatory Cytokine-induced Prothrombotic Molecules in Endothelial Cells

Paclitaxel Potentiates Inflammatory Cytokine-induced Prothrombotic Molecules in Endothelial Cells

Histamine H1 Receptor Promotes Atherosclerotic Lesion Formation by Increasing Vascular Permeability for Low-Density Lipoproteins

The Mast Cell, Contact, and Coagulation System Connection in Anaphylaxis

Contact Info

Product

Resources

About