Reperfusion-induced leukocyte adhesion and vascular protein leakage in normal and hypercholesterolemic rats

1997 ◽  
Vol 273 (2) ◽  
pp. H854-H860 ◽  
Author(s):  
I. Kurose ◽  
L. W. Argenbright ◽  
D. C. Anderson ◽  
J. Tolley ◽  
M. Miyasaka ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
Platelet Aggregation ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Leukocyte Adherence ◽  
Intercellular Adhesion Molecule 1 ◽  
Albumin Leakage ◽  
Endothelial Cell Adhesion

The objective of this study was to define the influence of hypercholesterolemia on ischemia-reperfusion (I/R)-induced leukocyte-endothelial cell adhesion and albumin leakage in rat mesenteric venules. The microvascular alterations normally elicited by I/R (leukocyte adherence and emigration, albumin leakage, and platelet aggregation) were more pronounced in hypercholesterolemic rats (compared with control rats). Monoclonal antibodies against the adhesion glycoproteins CD11/CD18 and intercellular adhesion molecule-1 attenuated the I/R-induced leukocyte adherence and emigration and albumin leakage. Leukocyte adherence, but not albumin leakage, was diminished in animals pretreated with a P-selectin-specific antibody. Platelet aggregation was reduced by antibodies directed against either P-selectin, CD18, or intercellular adhesion molecule-1, as well as a GPIIb-IIIa antagonist. These results indicate that the enhanced reperfusion-induced albumin leakage in hypercholesterolemic rats is dependent on leukocyte-endothelial cell adhesion. Furthermore, P-selectin- and CD11/CD18-dependent heterotypic and GPIIb-IIIa-mediated homotypic platelet aggregation appear to influence the extravasation of both leukocytes and albumin in postischemic venules of hypercholesterolemic rats.

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.

Postischemic endothelium-dependent vascular reactivity is preserved in adhesion molecule-deficient mice

1997 ◽  
Vol 273 (6) ◽  
pp. H2721-H2725 ◽  
Author(s):  
Michael A. Banda ◽  
David J. Lefer ◽  
D. Neil Granger
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
Adhesion Molecule ◽  
Vascular Reactivity ◽  
Cell Injury ◽  
Ischemia Reperfusion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Deficient Mice ◽  
Endothelial Cell Adhesion

Previous studies utilizing monoclonal antibodies directed against specific leukocyte-endothelial cell adhesion proteins have suggested that neutrophils mediate endothelial cell injury in a number of vascular beds after ischemia-reperfusion (I/R). In the present study, we investigated superior mesenteric artery (SMA) vascular reactivity to acetylcholine (ACh) and sodium nitroprusside (SNP) after occlusion and reperfusion in wild-type (C57BL/6) mice and in gene-targeted mice that are deficient in either CD11/CD18, intercellular adhesion molecule 1 (ICAM-1), or P-selectin. All mice were 4 wk of age, and the SMA was occluded for 45 min and then reperfused for 45 min. Segments of SMA were isolated and suspended in organ chambers and contracted with phenylephrine (10−5 M), and the maximal vasorelaxation to ACh (10−6 M) and SNP (10−6 M) was measured. SMA from sham-operated C57BL/6 mice relaxed 83.5 ± 3.3% to ACh and 91.7 ± 3.4% to SNP. In contrast, segments of SMA from C57BL/6 mice subjected to I/R demonstrated a marked impairment in vasorelaxation to ACh (51.3 ± 4.7%, P < 0.01 vs. sham) without any impairment in the vasoreactivity to SNP (86.1 ± 5.5%). In CD11/CD18-deficient mice, SMA reactivity to ACh (84.7 ± 2.3%) and SNP (91.2 ± 2.8%) was unaffected by I/R. Similarly, SMA rings from ICAM-1-deficient mice exhibited normal vasorelaxation to ACh and SNP with maximal vasorelaxation of 83.1 ± 2.9 and 87.4 ± 3.0%, respectively. We also observed profound preservation of endothelium-dependent vasorelaxation after I/R in P-selectin-deficient mice. These findings indicate that leukocyte-endothelial cell adhesion molecule deficiency is associated with the preservation of endothelium-dependent vascular responses after I/R.

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