Investigation of soluble adhesion molecules in cancer: beneficial approach or expensive toy? The case of intercellular adhesion molecule-1 (sICAM-1)

1994 ◽  
Vol 3 (0) ◽  
pp. 73
Author(s):  
Kay M. Reinhardt ◽  
Dagmar Zillig ◽  
W. Brinckmann ◽  
Beate Krammer ◽  
Andrew D. Blann ◽  
...  
Keyword(s):  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Soluble Adhesion Molecules ◽  
Beneficial Approach

Soluble Adhesion Molecules E-Cadherin, Intercellular Adhesion Molecule-1, and E-Selectin as Lung Cancer Biomarkers

CHEST Journal ◽  
2010 ◽  
Vol 138 (5) ◽  
pp. 1173-1179 ◽  
Author(s):  
Athena Gogali ◽  
Konstantinos Charalabopoulos ◽  
Iris Zampira ◽  
Athanasios K. Konstantinidis ◽  
Fanny Tachmazoglou ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cancer Biomarkers ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Soluble Adhesion Molecules ◽  
E Cadherin

Changes in leucocyte counts and soluble intercellular adhesion molecule-1 and E-selectin during cardiopulmonary bypass in children

Perfusion ◽  
1998 ◽  
Vol 13 (5) ◽  
pp. 322-327 ◽  
Author(s):  
Hilary J Williams ◽  
Naomi Rebuck ◽  
Martin J Elliott ◽  
Adam Finn
Keyword(s):  
Cardiopulmonary Bypass ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Plasma Concentrations ◽  
Endothelial Damage ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Soluble Adhesion Molecules ◽  
Cell Counts

A consequence of cardiopulmonary bypass (CPB) in young children is postoperative capillary leak and associated pulmonary dysfunction. Neutrophils sequester in the lungs and may contribute to functional endothelial damage. The endothelial adhesion molecules, E-selectin and intercellular adhesion molecule-1 (ICAM-1), mediate sequential steps in adhesion by binding to leucocyte ligands. Circulating forms of these proteins have been identified. We studied changes in the plasma concentrations of soluble E-selectin and soluble ICAM-1 using fixed phase immunoassays, and associated leucocyte counts in 10 paediatric patients undergoing CPB. Concentrations of soluble L-selectin and soluble ICAM-1 consistently fell during CPB from preoperative levels of 89 ± 17 ng/ml (mean ± 2SEM) and 218 + 61 ng/ml, respectively, to 39 ± 7 ng/ml and 84 ± 24 ng/ml, respectively at the beginning of maximum hypothermia. The haemodilution that occurred during CPB largely explained this fall, but not the more marked decrease in white cell counts that also occurred over this period (6.7 ± 1.1 to 1.7 ± 0.5 × 109/l) which may reflect increased leucocyte sequestration. By 24 h postoperatively, levels of both soluble adhesion molecules approached preoperative concentrations, as did lymphocyte counts. In marked contrast, neutrophil counts rose appreciably towards the end of CPB, and continued to rise to a maximum of 10.9 ± 3.1 ×109/l during the immediate postoperative period and remained at these elevated levels 24 h later. Major consistent changes in circulating leucocyte numbers which occur early in cardiopulmonary bypass may reflect changes in adhesion to the endothelium and consequent sequestration. Alterations in the levels of soluble adhesion proteins may influence these processes.

scholarly journals Role of poly(ADP-ribose) synthetase in pulmonary leukocyte recruitment

2003 ◽  
Vol 285 (5) ◽  
pp. L996-L1005 ◽  
Author(s):  
Rainer Kiefmann ◽  
Kai Heckel ◽  
Martina Dörger ◽  
Sonja Schenkat ◽  
Mechthild Stoeckelhuber ◽  
...  
Keyword(s):  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Leukocyte Recruitment ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Edema Formation ◽  
Pulmonary Microcirculation

During systemic inflammation, recruitment and activation of leukocytes in the pulmonary microcirculation may result in a potentially life-threatening acute lung injury. We elucidated the role of the poly(ADP-ribose) synthetase (PARS), a nucleotide-polymerizing enzyme, in the regulation of leukocyte recruitment within the lung with regard to the localization in the pulmonary microcirculation and in correlation to hemodynamics in the respective vascular segments and expression of intercellular adhesion molecule 1 during endotoxemia. Inhibition of PARS by 3-aminobenzamide reduced the endotoxin-induced leukocyte recruitment within pulmonary arterioles, capillaries, and venules in rabbits as quantified by in vivo fluorescence microscopy. Microhemodynamics and thus shear rates in all pulmonary microvascular segments remained constant. Simultaneously, inhibition of PARS with 3-aminobenzamide suppressed the endotoxin-induced adhesion molecules expression as demonstrated for intercellular adhesion molecule 1 by immunohistochemistry and Western blot analysis. We confirmed this result with the use of PARS knockout mice. The inhibitory effect of 3-aminobenzamide on leukocyte recruitment was associated with a reduction of pulmonary capillary leakage and edema formation. We first provide evidence that PARS activation mediates the leukocyte sequestration in pulmonary microvessels through upregulation of adhesion molecules. As reactive oxygen species released from leukocyte are supposed to cause an upregulation of adhesion molecules we conclude that PARS inhibition contributes to termination of this vicious cycle and inhibits the inflammatory process.

Lack of the adhesion molecules P-selectin and intercellular adhesion molecule-1 accelerate the development of BCR/ABL-induced chronic myeloid leukemia-like myeloproliferative disease in mice

Blood ◽  
2004 ◽  
Vol 104 (7) ◽  
pp. 2163-2171 ◽  
Author(s):  
Shawn D. Pelletier ◽  
Daniel S. Hong ◽  
Yiguo Hu ◽  
Yuhua Liu ◽  
Shaoguang Li
Keyword(s):  
Bone Marrow ◽  
Chronic Myeloid Leukemia ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Myeloid Leukemia ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Adhesion Properties ◽  
Marrow Stroma

Abstract In vitro studies show that BCR/ABL-expressing hematopoietic cells exhibit altered adhesion properties. No in vivo studies show whether the altered adhesion properties affect BCR/ABL leukemo-genesis. Using mice with homozygous inactivation of genes encoding the 2 adhesion molecules P-selectin and intercellular adhesion molecule-1 (ICAM1), we show that the mutant mice develop BCR/ABL-induced chronic myeloid leukemia (CML)-like leukemia at a significantly faster rate than do wild-type (WT) mice. Lack of P-selectin and ICAM1 did not have a significant effect on the development of B-cell acute lymphoblastic leukemia (BALL) induced by BCR/ABL. Using mice deficient for P-selectin or ICAM1 alone, we show that P-selectin plays a major role in the acceleration of CML-like leukemia. Lack of P-selectin resulted in early release of BCR/ABL-expressing myeloid progenitors from bone marrow, appearing to alter the biologic properties of leukemic cells rather than their growth rate by increasing their homing to the lungs, causing fatal lung hemorrhages. These results indicate that adhesion of BCR/ABL-expressing myeloid progenitors to marrow stroma through P-selectin and ICAM1 play an inhibitory role in the development of CML-like disease, suggesting that improvement of adhesion between BCR/ABL-expressing myeloid progenitor cells and bone marrow stroma may be of therapeutic value for human CML. (Blood. 2004;104:2163-2171)

Attenuation of experimental subarachnoid hemorrhage–induced increases in circulating intercellular adhesion molecule–1 and cerebral vasospasm by the endothelin-converting enzyme inhibitor CGS 26303

2007 ◽  
Vol 106 (3) ◽  
pp. 442-448 ◽  
Author(s):  
Chih-Lung Lin ◽  
Aij-Lie Kwan ◽  
Aaron S. Dumont ◽  
Yu-Feng Su ◽  
Neal F. Kassell ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Autologous Blood ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Healthy Controls ◽  
Intercellular Adhesion Molecule 1 ◽  
Mediators Of Inflammation ◽  
Basilar Arteries

Object Adhesion molecules, including intercellular adhesion molecule–1 (ICAM-1), vascular cell adhesion molecule–1 (VCAM-1), and E-selectin, are important mediators of inflammation, and their levels are elevated in the serum of patients following aneurysmal subarachnoid hemorrhage (SAH). The investigators previously found that CGS 26303 is effective in preventing and reversing arterial narrowing in a rabbit model of SAH. The purpose of the present study was to examine whether levels of adhesion molecules are altered after treatment with CGS 26303 in this animal model. Methods New Zealand White rabbits were each injected with 3 ml of autologous blood in the cisterna magna, and intravenous treatment with CGS 26303 (30 mg/kg) was initiated 1 hour later. The compound was subsequently administered at 12, 24, and 36 hours post-SAH. Blood samples were collected at 48 hours post-SAH to measure ICAM-1, VCAM-1, and E-selectin levels. After the rabbits had been killed by perfusion–fixation, the basilar arteries (BAs) were removed and sliced, and their cross-sectional areas were measured. Treatment with CGS 26303 attenuated arterial narrowing after SAH. Morphologically, corrugation of the internal elastic lamina of BAs was prominently observed in the SAH only and vehicle-treated SAH groups, but not in the CGS 26303–treated SAH group or in healthy controls. There were no significant differences in the levels of VCAM-1 among the four groups. The levels of E-selectin were increased in all animals subjected to SAH (those in the SAH only, SAH plus vehicle, and SAH plus CGS 26303 groups) compared with healthy controls (no SAH); however, the levels of ICAM-1 in the SAH only and SAH plus vehicle groups were significantly elevated (p < 0.001), and treatment with CGS 26303 reduced ICAM-1 to control levels following SAH. Conclusions These results show that ICAM-1 may play a role in mediating SAH-induced vasospasm and that a reduction of ICAM-1 levels after SAH may partly contribute to the antispastic effect of CGS 26303.

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