Endothelial cell adhesion molecules in inflammation and postischemic reperfusion injury

Beekhuizen, Henry; Gevel, Joke S. van de

doi:10.1016/s0041-1345(98)01405-5

Cited by 27 publications

(33 citation statements)

References 56 publications

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“…In addition, we show that increased adhesion of monocytes to EC stimulated with rIL-1 for 24 h did not generate an increase in TFA during subsequent coculture. Analogous to experiments with 24-h TNF-␣-stimulated EC (24), this lack of TFA induction could be explained, at least in part, by the absence of E-selectin (CD62E) molecules on the surfaces of rIL-1-stimulated EC (10). These molecules augment monocyte-EC interaction and were shown to mediate TFA induction during subsequent coculture of these cells (24).…”

Section: Discussionmentioning

confidence: 75%

Monocytes Augment Bacterial Species- and Strain-Dependent Induction of Tissue Factor Activity in Bacterium-Infected Human Vascular Endothelial Cells

2001

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In bacterial endocarditis (BE), intravascular infection with Staphylococcus aureus, Streptococcus sanguis, orStaphylococcus epidermidis can lead to formation of a fibrin clot on the inner surface of the heart and cause heart dysfunction. The events that start the coagulation in the early stage of the disease are largely unknown. We have recently shown that human endothelial cells (EC) upon binding and internalization of S. aureus, but not S. sanguis or S. epidermidis, express tissue factor (TF)-dependent procoagulant activity (TFA). The present study shows that infection of EC with these three pathogens induces surface expression of intracellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) and monocyte adhesion. Subsequent coculture of these cells synergistically enhanced TFA, which was exclusively dependent on TF molecules that were expressed on EC during coculture. TFA induction required direct contact between monocytes and bacterium-infected EC, but the signals for this response were not generated by the binding of monocytes through their ␤ 2 -or ␣ 4 -integrins to ICAM-1 or VCAM-1, respectively, on infected EC. The mechanism by which monocytes induce TFA in bacterium-infected EC was partly mediated by the proinflammatory cytokine interleukin-1 produced by the cells during coculture. Endogenous tumor necrosis factor alpha was not involved. This modulating effect of monocytes on species-and strain-dependent TFA of bacterium-infected EC supports our hypothesis that in an early stage in the pathogenesis of BE, as well as other intravascular infections that lead to detrimental fibrin formation, the coagulation cascade can be activated on the surfaces of EC as a consequence of specific interactions between pathogenic bacteria, EC, and monocytes.

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Section: Discussionmentioning

confidence: 75%

Monocytes Augment Bacterial Species- and Strain-Dependent Induction of Tissue Factor Activity in Bacterium-Infected Human Vascular Endothelial Cells

2001

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“…Neutrophil-endothelial interactions are the initial event involved in the onset of inflammatory diseases. 1 Especially in ischemia/reperfusion (I/R) injuries, circulating neutrophils selectively infiltrate ischemic tissues and contribute to tissue destruction. [2][3][4] During the progression of I/R injuries, endothelial barrier is impaired within a few hours by hypoxia or neutrophil-released toxic products.…”

Section: Ischemia and Reperfusion (I/r) Injuries Occur In Numerous Ormentioning

confidence: 99%

Prevention of Neutrophil Extravasation by Hepatocyte Growth Factor Leads to Attenuations of Tubular Apoptosis and Renal Dysfunction in Mouse Ischemic Kidneys

Mizuno

Nakamura

2005

The American Journal of Pathology

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“…It has also been shown that polymorphonuclear leukocytes (PMNs), one type of inflammatory cells, contribute to endothelial cell dysfunction by the release of inflammatory mediators such as ROS and hydrolytic mediators (11). However, the physiological function of PMNs on TF activity in endothelial cells is still unclear.…”

mentioning

confidence: 99%

Changes of Tissue Factor-Dependent Coagulant Activity Mediated by Adhesion Between Polymorphonuclear Leukocytes and Endothelial Cells

Watanabe

Tokuyama

Yasuda

et al. 2001

Japanese Journal of Pharmacology

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ABSTRACT-The purpose of this study was to examine whether polymorphonuclear leukocytes (PMNs) facilitate a tissue factor, a physiologic initiator of coagulation in endothelial cells, -dependent coagulant activity (TF activity). The TF activity in bovine endothelial cells (BAECs) was significantly increased in a concentration-dependent manner by PMNs (1´10 5 -1´10 7 cells/ ml) without affecting the treatment of Nformyl-methionyl-leucyl-phenylalanine, a selective activator of PMNs, and the addition of PMNs finally resulted in cell damage as evaluated by the lactate dehydrogenase leakage method. In the same conditions, an increase of adhesion between PMNs and BAECs was also observed in a time-dependent manner. However, since direct adhesion of PMNs to BAECs was impossible by using the transwell, PMNs failed to induce any changes in the TF activity. Hence, the change of TF activity found here might be closely related to the PMNs adhesion to BAECs. Indeed, anti-intercellular adhesion molecule-1 (anti-ICAM-1) antibody blocked the increase of TF activity in BAECs. These findings suggest that PMNs could increase TF activity in endothelial cells, which is triggered by adhesion to endothelial cells through ICAM-1.

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Endothelial cell adhesion molecules in inflammation and postischemic reperfusion injury

Cited by 27 publications

References 56 publications

Monocytes Augment Bacterial Species- and Strain-Dependent Induction of Tissue Factor Activity in Bacterium-Infected Human Vascular Endothelial Cells

Monocytes Augment Bacterial Species- and Strain-Dependent Induction of Tissue Factor Activity in Bacterium-Infected Human Vascular Endothelial Cells

Prevention of Neutrophil Extravasation by Hepatocyte Growth Factor Leads to Attenuations of Tubular Apoptosis and Renal Dysfunction in Mouse Ischemic Kidneys

Changes of Tissue Factor-Dependent Coagulant Activity Mediated by Adhesion Between Polymorphonuclear Leukocytes and Endothelial Cells

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