VCAM-1 is more effective than MAdCAM-1 in supporting eosinophil rolling under conditions of shear flow

Blood ◽  
2000 ◽  
Vol 95 (2) ◽  
pp. 592-601 ◽  
Author(s):  
P. Sriramarao ◽  
Richard G. DiScipio ◽  
Ronald R. Cobb ◽  
Myron Cybulsky ◽  
Greg Stachnick ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Parallel Plate ◽  
Cell Adhesion Molecule ◽  
Flow Chamber ◽  
Β1 Integrin ◽  
Vascular Cell Adhesion ◽  
Parallel Plate Flow Chamber ◽  
Vascular Cell

The ability of the 4 integrin counterligands vascular cell adhesion molecule (VCAM)-1 or mucosal addressin (MAd)CAM-1 to support eosinophil rolling or firm adhesion under conditions of physiologic flow has not been delineated. Using a parallel plate flow chamber in vitro and intravital microscopy in vivo, we demonstrate that eosinophil rolling and adhesion on VCAM-1 is mediated by both 4β1 and 4β7 integrins. Eosinophils rolled equally efficiently on both VCAM-1 2 domain and VCAM-1 7 domain, suggesting that the N-terminal 2 domains of VCAM-1 are sufficient to support eosinophil rolling under conditions of flow. Furthermore, activation of the eosinophil β1 integrin with monoclonal antibody (mAb) 8A2 resulted in both resistance to shear stress–induced detachment from VCAM-1 in vitro and in stable arrest of rolling eosinophils on interleukin (IL)-1β–stimulated venules in vivo. Eosinophils rolled less efficiently on MAdCAM-1– than on VCAM-1–coated coverslips under conditions of flow. However, eosinophils firmly adhered as efficiently to MAdCAM-1 as to VCAM-1. Overall, these results demonstrate that both VCAM-1 and MAdCAM-1 can support eosinophil firm adhesion under conditions of flow. In contrast, VCAM-1 is significantly more efficient than MAdCAM-1 in supporting eosinophil rolling under conditions of flow.

scholarly journals A fluid–structure interaction model to characterize bone cell stimulation in parallel-plate flow chamber systems

2013 ◽  
Vol 10 (81) ◽  
pp. 20120900 ◽  
Author(s):  
T. J. Vaughan ◽  
M. G. Haugh ◽  
L. M. McNamara
Keyword(s):  
Shear Stress ◽  
Fluid Flow ◽  
Parallel Plate ◽  
Bone Cells ◽  
Mechanical Stimulus ◽  
Flow Chamber ◽  
Parallel Plate Flow Chamber ◽  
Structure Interaction

Bone continuously adapts its internal structure to accommodate the functional demands of its mechanical environment and strain-induced flow of interstitial fluid is believed to be the primary mediator of mechanical stimuli to bone cells in vivo. In vitro investigations have shown that bone cells produce important biochemical signals in response to fluid flow applied using parallel-plate flow chamber (PPFC) systems. However, the exact mechanical stimulus experienced by the cells within these systems remains unclear. To fully understand this behaviour represents a most challenging multi-physics problem involving the interaction between deformable cellular structures and adjacent fluid flows. In this study, we use a fluid–structure interaction computational approach to investigate the nature of the mechanical stimulus being applied to a single osteoblast cell under fluid flow within a PPFC system. The analysis decouples the contribution of pressure and shear stress on cellular deformation and for the first time highlights that cell strain under flow is dominated by the pressure in the PPFC system rather than the applied shear stress. Furthermore, it was found that strains imparted on the cell membrane were relatively low whereas significant strain amplification occurred at the cell–substrate interface. These results suggest that strain transfer through focal attachments at the base of the cell are the primary mediators of mechanical signals to the cell under flow in a PPFC system. Such information is vital in order to correctly interpret biological responses of bone cells under in vitro stimulation and elucidate the mechanisms associated with mechanotransduction in vivo .

scholarly journals Effects of insulin on in vitro vascular cell adhesion molecule-1 expression and in vivo soluble VCAM-1 release

Diabetologia ◽  
1999 ◽  
Vol 42 (10) ◽  
pp. 1235-1239 ◽  
Author(s):  
G. De Mattia ◽  
M. C. Bravi ◽  
A. Costanzo ◽  
O. Laurenti ◽  
M. Cassone Faldetta ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Vascular Cell Adhesion ◽  
Vascular Cell ◽  
Vascular Cell Adhesion Molecule ◽  
Cell Adhesion Molecule 1

scholarly journals JAK2-V617F activates β1-integrin-mediated adhesion of granulocytes to vascular cell adhesion molecule 1

Leukemia ◽  
2017 ◽  
Vol 31 (5) ◽  
pp. 1223-1226 ◽  
Author(s):  
N Gupta ◽  
B Edelmann ◽  
T M Schnoeder ◽  
F C Saalfeld ◽  
D Wolleschak ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Jak2 V617f ◽  
Β1 Integrin ◽  
Vascular Cell Adhesion ◽  
Vascular Cell ◽  
Vascular Cell Adhesion Molecule ◽  
Cell Adhesion Molecule 1

Airway recruitment of leukocytes in mice is dependent on alpha4-integrins and vascular cell adhesion molecule-1

1997 ◽  
Vol 272 (2) ◽  
pp. L219-L229 ◽  
Author(s):  
J. E. Chin ◽  
C. A. Hatfield ◽  
G. E. Winterrowd ◽  
J. R. Brashler ◽  
S. L. Vonderfecht ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Pulmonary Inflammation ◽  
Vascular Cell Adhesion ◽  
Vascular Cell ◽  
Vascular Cell Adhesion Molecule ◽  
Cell Adhesion Molecule 1

The involvement of the alpha4-integrin very late activation antigen 4 and vascular cell adhesion molecule-1 (VCAM-1) in leukocyte trafficking into the airways of ovalbumin (OA)-sensitized and OA-challenged mice was investigated using in vivo administration of anti-alpha4 monoclonal antibodies (mAb) PS/2, R1-2, and M/K-2.7 (MK2), specific for VCAM-1. VCAM-1 was upregulated on endothelial cells in lung tissue after OA inhalation. PS/2, R1-2, or MK2 significantly inhibited the recruitment of eosinophils and lymphocytes into the bronchoalveolar lavage (BAL) fluid and decreased inflammation in the lung tissues. Escalating in vivo doses of PS/2 or MK2 increased circulating levels of rat immunoglobulin G in the plasma. The binding of phycoerytherin-labeled anti-alpha4 mAb to blood T cells from PS/2-treated mice was reduced, implying that alpha4 sites were already occupied. T cells and eosinophils in BAL fluid from mice treated with PS/2 or MK2 were phenotypically different from controls. Selective decreases of alpha4+ T cells in the BAL fluid after PS/2 or MK2 treatment were coupled with changes in CD8+, CD11a, and CD62L expression. The alpha4-integrin and VCAM-1 may have important roles in the antigen-induced recruitment of T cells and eosinophils during OA-induced airway inflammation. The data suggest that these adhesion molecules may be suitable targets for therapeutic intervention in certain conditions of pulmonary inflammation.

α-Lipoic acid reduces expression of vascular cell adhesion molecule-1 and endothelial adhesion of human monocytes after stimulation with advanced glycation end products

1999 ◽  
Vol 96 (1) ◽  
pp. 75-82 ◽  
Author(s):  
Thomas KUNT ◽  
Thomas FORST ◽  
Axel WILHELM ◽  
Hans TRITSCHLER ◽  
Andreas PFUETZNER ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Lipoic Acid ◽  
Cell Adhesion Molecule ◽  
Vascular Cell Adhesion ◽  
Advanced Glycation ◽  
Vascular Cell ◽  
Glycation End Products ◽  
End Products ◽  
Cell Adhesion Molecule 1

Advanced glycation end products (AGEs) have been identified as relevant mediators of late diabetic complications such as atherosclerotic disease. The endothelial migration of monocytes is one of the first steps in atherogenesis and monocyte–endothelial interaction itself is linked to the expression of adhesion molecules like vascular cell adhesion molecule-1 (VCAM-1). Recently, stimulation of VCAM-1 by AGEs has been demonstrated. Since endothelial stimulation by AGEs is followed by generation of oxygen free radicals with subsequent activation of nuclear transcription factor κB, we investigated the influence of α-lipoic acid on the expression of VCAM-1 and monocyte adherence to endothelial cells in vitro by means of cell-associated chemiluminescence assays and quantitative reverse transcriptase polymerase chain reaction using a constructed recombinant RNA standard. We found that α-lipoic acid was able to decrease the number of VCAM-1 transcripts from 41.0±11.2 to 9.5±4.7 RNA copies per cell in AGE-stimulated cell cultures. Furthermore, expression of VCAM-1 was suppressed in a time- and dose-dependent manner by α-lipoic acid as shown by chemiluminescence endothelial cell assay. Pretreatment of endothelial cells with 0.5 ;mM or 5 ;mM α-lipoic acid reduced AGE-induced endothelial binding of monocytes from 22.5±2.9% to 18.3±1.9% and 13.8±1.8% respectively. Thus, we suggest that extracellularly administered α-lipoic acid reduces AGE-albumin-induced endothelial expression of VCAM-1 and monocyte binding to endothelium in vitro. These in vitro results may contribute to the understanding of a potential antioxidative treatment of atherosclerosis.

scholarly journals Chemoattractants Induce a Rapid and Transient Upregulation of Monocyte α4 Integrin Affinity for Vascular Cell Adhesion Molecule 1 Which Mediates Arrest

2001 ◽  
Vol 193 (10) ◽  
pp. 1149-1158 ◽  
Author(s):  
Jason R. Chan ◽  
Sharon J. Hyduk ◽  
Myron I. Cybulsky
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Platelet Activating Factor ◽  
Flow Chamber ◽  
Blood Monocytes ◽  
Vascular Cell Adhesion ◽  
Vascular Cell ◽  
Vascular Cell Adhesion Molecule ◽  
Stromal Cell Derived Factor

Chemoattractants and chemokines induce arrest of rolling monocytes during emigration from blood into tissues. In this study, we demonstrated that α4 integrin affinity for vascular cell adhesion molecule (VCAM)-1 was upregulated rapidly and transiently by chemoattractants and stromal cell–derived factor (SDF)-1α and mediated monocyte arrest. α4 integrin affinity changes were detected and blocked using soluble VCAM-1/Fc (sVCAM-1/Fc). In a flow cytometry assay, markedly increased sVCAM-1/Fc binding to human blood monocytes or U937 cells transfected with formyl peptide (FP) receptor was detected 30 s after FP or SDF-1α treatment and declined after 2 min. In a parallel plate flow chamber assay, FP, C5a, platelet-activating factor, or SDF-1α coimmobilized with VCAM-1 induced leukocyte arrest, which was blocked by inclusion of sVCAM-1/Fc but not soluble nonimmune immunoglobulin G in the assay buffer.

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