Adhesion molecules contribute to ischemia and reperfusion-induced injury in the isolated rat lung

1995 ◽  
Vol 78 (6) ◽  
pp. 2245-2252 ◽  
Author(s):  
T. M. Moore ◽  
P. Khimenko ◽  
W. K. Adkins ◽  
M. Miyasaka ◽  
A. E. Taylor
Keyword(s):  
Endothelial Cell ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Leukocyte Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Ischemia And Reperfusion ◽  
Intercellular Adhesion Molecule 1 ◽  
Endothelial Cell Adhesion Molecules ◽  
Permeability Increase ◽  
Isolated Rat Lung

Leukocyte adherence to the endothelium after ischemia and reperfusion contributes to microvascular injury in most organs. The purpose of this study was to evaluate the leukocyte and endothelial cell adhesion molecules involved with ischemia-reperfusion (I/R)-induced pulmonary microvascular injury in the isolated rat lung. After 45 min of ischemia and 30 min of reperfusion, microvascular permeability was significantly increased and lung retention of leukocytes occurred. Pretreatment with monoclonal antibodies against the leukocyte adhesion molecule CD18 or the endothelial cell adhesion molecules intercellular adhesion molecule 1 and P-selectin significantly attenuated the I/R-induced permeability increase and lung sequestration of neutrophils, mononuclear leukocytes, and eosinophils. In contrast, immunoneutralization of the rat leukocyte adhesion molecule L-selectin neither protected against the I/R-induced permeability increase nor prevented lung sequestration of neutrophils and eosinophils. We conclude that leukocyte adherence in the pulmonary, microvasculature and subsequent permeability increase after I/R is dependent on the integrin CD18, its endothelial cell ligand intercellular adhesion molecule 1, and the endothelial cell rolling factor P-selectin but not the leukocyte rolling factor L-selectin.

scholarly journals Elevated Expression of Serum Endothelial Cell Adhesion Molecules in COVID-19 Patients

2020 ◽  
Vol 222 (6) ◽  
pp. 894-898 ◽  
Author(s):  
Ming Tong ◽  
Yu Jiang ◽  
Da Xia ◽  
Ying Xiong ◽  
Qing Zheng ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecules ◽  
Serum Levels ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Endothelial Cell Adhesion Molecules ◽  
Endothelial Cell Adhesion

Abstract In a retrospective study of 39 COVID-19 patients and 32 control participants in China, we collected clinical data and examined the expression of endothelial cell adhesion molecules by enzyme-linked immunosorbent assays. Serum levels of fractalkine, vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), and vascular adhesion protein-1 (VAP-1) were elevated in patients with mild disease, dramatically elevated in severe cases, and decreased in the convalescence phase. We conclude the increased expression of endothelial cell adhesion molecules is related to COVID-19 disease severity and may contribute to coagulation dysfunction.

Circulating Endothelial Cell/Leukocyte Adhesion Molecules in Atherosclerosis

1994 ◽  
Vol 72 (01) ◽  
pp. 151-154 ◽  
Author(s):  
Andrew D Blann ◽  
Charles N McCollum
Keyword(s):  
Endothelial Cell ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cell Activation ◽  
Leukocyte Adhesion ◽  
Clinical Manifestations ◽  
Intercellular Adhesion Molecule ◽  
Endothelial Cell Activation ◽  
Soluble Adhesion Molecules ◽  
Von Willebrand

SummarySoluble adhesion molecules E-selectin, intercellular adhesion molecule (sICAM) and vascular cell adhesion molecule (sVCAM) were measured alongside von Willebrand factor (vWf) in 40 patients with peripheral vascular disease (PVD), 43 with ischaemic heart disease (IHD) and in equal numbers of age and sex matched asymptomatic controls. Increased vWf was found in patients with IHD (p = 0.0008) and in patients with PVD (p = 0.0001) relative to their respective controls but levels did not differ between the two patient groups. Raised sICAM was found in both PVD (p = 0.0003) and IHD (p = 0.0059) compared to their respective controls and was higher in PVD than in IHD (p = 0.0088). In the subjects taken as a whole, there was no correlation between vWf and sICAM. Levels of soluble E-sel-ectin and sVCAM did not differ in patients or controls. These data suggest that soluble ICAM may be useful as an index of endothelial cell activation in clinical manifestations of atherosclerosis.

scholarly journals The Cytolytically Inactive Terminal Complement Complex Activates Endothelial Cells to Express Adhesion Molecules and Tissue Factor Procoagulant Activity

1997 ◽  
Vol 185 (9) ◽  
pp. 1619-1628 ◽  
Author(s):  
Francesco Tedesco ◽  
Mario Pausa ◽  
Ermanno Nardon ◽  
Martino Introna ◽  
Alberto Mantovani ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tissue Factor ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Leukocyte Adhesion ◽  
Membrane Attack Complex ◽  
Procoagulant Activity ◽  
Biologically Active ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1

The membrane attack complex of complement (C) in sublytic concentrations stimulates endothelial cells (EC) to express adhesion molecules and to release biologically active products. We have examined the ability of a cytolytically inactive form of this complex, which is incapable of inserting into the cell membrane, to upregulate the expression of adhesion molecules and of tissue factor (TF) procoagulant activity. The inactive terminal C complex (iTCC) was prepared by mixing C5b6, C7, C8, and C9 and was purified by fast protein liquid chromatography on a Superose 12 column. Binding of this complex to EC was found to be dose dependent and was inhibited by anti-C9 antibodies, as assessed both by ELISA using an mAb anti-C9 neoantigen and by measuring cell-bound 125I-labeled iTCC. Exposure of EC to iTCC resulted in a dose- and time-dependent expression of endothelial leukocyte adhesion molecule 1, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 accompanied by increased levels of the corresponding mRNA, but not in the rapid expression of P-selectin. Inactive TCC also induced increased TF activity evaluated by a chromogenic assay that measures the formation of factor Xa. These effects were inhibited by anti-C9 antibodies. The data support the conclusion that iTCC may induce proinflammatory and procoagulant activities on EC.

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