Role of Tyrosine Kinase Enzymes in TNF‐α and IL‐1 Induced Expression of ICAM‐1 and VCAM‐1 on Human Umbilical Vein Endothelial Cells

Majewska, Ewelina; Paleolog, Ewa; Baj, Zbigniew; Kralisz, Urszula; Feldmann, M; Tchórzewski, H

doi:10.1046/j.1365-3083.1997.d01-412.x

Cited by 35 publications

(27 citation statements)

References 40 publications

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“…CBMCs do not produce any detectable IL-1␤ (Ͻ3.9 pg/ml) following antibody-enhanced dengue virus infection (data not shown). Previous reports have indicated that (20 ng/ml) IL-1␤ induces HUVEC upregulation (31). Importantly, these reported levels are at least 1,000 times higher than those produced by HMC-1 cells and CBMCs.…”

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confidence: 80%

Dengue Virus Infection of Mast Cells Triggers Endothelial Cell Activation

Brown

Hermann

Issekutz

et al. 2011

J Virol

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Vascular perturbation is a hallmark of severe forms of dengue disease. We show here that antibodyenhanced dengue virus infection of primary human cord blood-derived mast cells (CBMCs) and the human mast cell-like line HMC-1 results in the release of factor(s) which activate human endothelial cells, as evidenced by increased expression of the adhesion molecules ICAM-1 and VCAM-1. Endothelial cell activation was prevented by pretreatment of mast cell-derived supernatants with a tumor necrosis factor (TNF)-specific blocking antibody, thus identifying TNF as the endothelial cell-activating factor. Our findings suggest that mast cells may represent an important source of TNF, promoting vascular endothelial perturbation following antibody-enhanced dengue virus infection.Dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) represent the most life-threatening clinical outcomes of dengue virus infections. The immunopathological mechanisms are significant and include antibody-dependent enhancement of dengue virus infection, a known risk factor in the development of DHF/DSS (18). A major distinguishing feature of DHF/DSS is plasma leakage; therefore, much attention has been directed to mechanisms of vascular endothelial dysfunction. Histological damage to the vascular endothelium in DHF cases is usually limited to swelling and occasional intercellular gaps (41), suggesting that endothelial perturbation is mediated by subtle immunopathological effects rather than by cytopathological virus infection. Dengue virus infection promotes upregulation of membrane-associated and soluble adhesion molecules which are indicative of endothelial cell activation (1, 36). These parameters correlate with disease severity (9,21,25,34,43).Mast cells are connective tissue-associated leukocytes located at areas of external interface, such as the skin and mucous membranes. They are in close proximity to blood vessels, with functional roles in a variety of inflammatory conditions (i.e., asthma and allergy) and innate protection against pathogens. The evidence for mast cell involvement in dengue disease includes observations that dengue patients exhibit increased levels of blood and urinary histamine (a product of mast cells and basophils), which correlates with disease severity (37,47). A large histological study of DHF patients noted that mast cells in the connective tissue around the thymus showed swelling, vacuolation of the cytoplasm, and loss of granule integrity, suggestive of mast cell activation (5). Mast cells are also involved in skin eruptions (rash), a common feature of dengue virus infection (19,35,42,48).We have previously reported that human mast cells are permissive to antibody-enhanced dengue virus infection, occurring in an Fc␥RII-dependent manner (6, 23). Infection of mast cell lines KU812 and HMC-1 results in infectious virus production and the induction of significant levels of cytokines, such as interleukin-1␤ (IL-1␤) and IL-6, as well as chemokines CCL3, CCL4, and CCL5, which can recruit additional immune effector...

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confidence: 80%

Dengue Virus Infection of Mast Cells Triggers Endothelial Cell Activation

Brown

Hermann

Issekutz

et al. 2011

J Virol

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“…It was also demonstrated that genistein inhibits lipopolysaccharide-stimulated TNF-production in a macrophage cell line [104] and TNF-levels in vivo [105]. Genistein also dosedependently inhibits TNF--induced MCP-1, ICAM-1 ,VCAM-1 [106][107][108] and matrix metalloproteinases (MMPs) [109] secretion both in vitro and in vivo, and the proliferation of VSMCs from spontaneously hypertensive rats [110].…”

Section: Genistein and Vascular Inflammationmentioning

confidence: 99%

Phytochemical Genistein in the Regulation of Vascular Function: New Insights

Liu²

2007

CMC

105

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Genistein, a natural bioactive compound derived from legumes, has drawn wide attention during the last decade because of its potentially beneficial effects on some human degenerative diseases. It has a weak estrogenic effect and is a well-known non-specific tyrosine kinase inhibitor at pharmacological doses. Epidemiological studies show that genistein intake is inversely associated with the risk of cardiovascular diseases. Data from animal and in vitro studies suggest a protective role of genistein in cardiovascular events. However, the mechanisms of the genistein action on vascular protective effects are unclear. Past extensive studies exploring its hypolipidemic effect resulted in contradictory data. Genistein also is a relatively poor antioxidant. However, genistein protects against pro-inflammatory factor-induced vascular endothelial barrier dysfunction and inhibits leukocyte-endothelium interaction, thereby modulating vascular inflammation, a major event in the pathogenesis of atherosclerosis. Recent studies found that genistein exerts a novel non-genomic action by targeting on important signaling molecules in vascular endothelial cells (ECs). Genistein rapidly activates endothelial nitric oxide synthase and production of nitric oxide in ECs. This genistein effect is novel since it is independent of its known effects, but mediated by the cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) cascade. Further studies demonstrated that genistein directly stimulates the plasma membrane-associated adenylate cyclases, leading to activation of the cAMP signaling pathway. In addition, genistein activates peroxisome proliferator-activated receptors, ligand-activated nuclear receptors important to normal vascular function. Furthermore, genistein reduces reactive oxygen species (ROS) by attenuating the expression of ROS-producing enzymes. These new findings reveal the novel roles for genistein in the regulation of vascular function and provide a basis for further investigating its therapeutic potential for inflammatory-related vascular disease.

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“…According to Collins et al [6], the strong positivity on stimulated HUVEC can be explained by induction of ICAM-1 gene expression by TNF·. For Majewska et al [46] the costimulatory effect of TNF-· in combination with protein tyrosine kinase inhibitors on ICAM-1 expression suggests an intracellular pathway of TNF-·-induced ICAM-1 expression, possibly involving downregulation of increases in ICAM-1 by protein tyrosine kinase enzyme.…”

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confidence: 99%

Comparative Analysis of the Reactivity of Human Umbilical Vein Endothelial Cells in Organ and Monolayer Culture

et al. 1999

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Endothelial monolayer cell cultures have been used to study pathomechanisms under standardized in vitro conditions. These results can only be regarded as valid as long as phenomena studied in vitro are comparable to findings in situ, e.g. in organ culture. The aim of the present study was to examine the reliability and comparability between human umbilical vein endothelial cells (HUVEC) in a monolayer cell culture model and endothelial cells (EC) in organ culture, as well as in the native umbilical cord. Our results prove the reliability of HUVEC as a model for standardized investigations of EC. The differences found suggest that gradual differences in antigen expression in vitro and in situ become apparent by comparing in situ and in vitro investigations.

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Role of Tyrosine Kinase Enzymes in TNF‐α and IL‐1 Induced Expression of ICAM‐1 and VCAM‐1 on Human Umbilical Vein Endothelial Cells

Cited by 35 publications

References 40 publications

Dengue Virus Infection of Mast Cells Triggers Endothelial Cell Activation

Dengue Virus Infection of Mast Cells Triggers Endothelial Cell Activation

Phytochemical Genistein in the Regulation of Vascular Function: New Insights

Comparative Analysis of the Reactivity of Human Umbilical Vein Endothelial Cells in Organ and Monolayer Culture

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