Quantitative investigations of the adhesiveness of circulating polymorphonuclear leucocytes to blood vessel walls

Atherton, A.; Born, G. V. R.

doi:10.1113/jphysiol.1972.sp009808

Cited by 351 publications

(157 citation statements)

References 14 publications

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“…For reasons that are not well elucidated, endothelial-leukocyte interaction and leukocyte emigration into the tissues is primarily concentrated in small vessels such as capillaries and post-capillary venules (8,9). This microvascular localization of endothelial-leukocyte interaction is only partially explained by the lower intensity of the hemodynamic shear forces in smaller vessels, which, in terms of possible mechanical interference, may be more conducive to leukocyte binding to the vessel wall than the higher shear intensities seen in the arterial trunks (7,12). The magnitude of shear stress in capillaries and post-capillary venules is Յ5 dynes/cm 2 (Յ0.5 pascal), which is significantly lower than the 10 -30 dynes/cm 2 (1-3 pascals) in arteries (13).…”

mentioning

confidence: 99%

Low Intensity Shear Stress Increases Endothelial ELR+ CXC Chemokine Production via a Focal Adhesion Kinase-p38β MAPK-NF-κB Pathway

Shaik

Soltau

Chaturvedi

et al. 2009

Journal of Biological Chemistry

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CXC chemokines with a glutamate-leucine-arginine (ELR) tripeptide motif (ELR؉ CXC chemokines) play an important role in leukocyte trafficking into the tissues. For reasons that are not well elucidated, circulating leukocytes are recruited into the tissues mainly in small vessels such as capillaries and venules. Because ELR ؉ CXC chemokines are important mediators of endothelial-leukocyte interaction, we compared chemokine expression by microvascular and aortic endothelium to investigate whether differences in chemokine expression by various endothelial types could, at least partially, explain the microvascular localization of endothelial-leukocyte interaction. Both in vitro and in vivo models indicate that ELR ؉ CXC chemokine expression is higher in microvascular endothelium than in aortic endothelial cells. These differences can be explained on the basis of the preferential activation of endothelial chemokine production by low intensity shear stress. Low shear activated endothelial ELR ؉ CXC chemokine production via cell surface heparan sulfates, ␤ 3 -integrins, focal adhesion kinase, the mitogen-activated protein kinase p38␤, mitogen-and stress-associated protein kinase-1, and the transcription factor.

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mentioning

confidence: 99%

Low Intensity Shear Stress Increases Endothelial ELR+ CXC Chemokine Production via a Focal Adhesion Kinase-p38β MAPK-NF-κB Pathway

Shaik

Soltau

Chaturvedi

et al. 2009

Journal of Biological Chemistry

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“…Pro-inflammatory stimuli promote tethering, rolling, and subsequent firm adhesion of leukocytes to the luminal vessel wall (5). These effects are mediated by the concerted action of endothelial cell selectins and the Ig adhesion molecules VCAM and ICAM (6).…”

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confidence: 99%

A Novel Protein with Homology to the Junctional Adhesion Molecule

Cunningham¹,

Arrate²,

Rodríguez³

et al. 2000

Journal of Biological Chemistry

143

117

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We have cloned a novel cDNA belonging to the Ig superfamily that shows 44% similarity to the junctional adhesion molecule (JAM) and maps to chromosome 21q21.2. The open reading frame of JAM2 predicts a 34-kDa type I integral membrane protein that features two Ig-like folds and three N-linked glycosylation sites in the extracellular domain. A single protein kinase C phosphorylation consensus site and a PDZ-binding motif are present in the short intracellular tail. Heterologous expression of JAM2 in Chinese hamster ovary cells defined a 48-kDa protein that localizes predominantly to the intercellular borders. Northern blot analysis showed that JAM2 is preferentially expressed in the heart. JAM2 homotypic interactions were demonstrated by the ability of JAM2-Fc to capture JAM2-expressing Chinese hamster ovary cells. We further showed that JAM2, but not JAM1, is capable of adhering to the HSB and HPB-ALL lymphocyte cell lines. Neutralizing mouse anti-JAM2 polyclonal antibodies provided evidence against homotypic interactions in this assay. Biotinylation of HSB cell membranes revealed a 43-kDa counterreceptor that precipitates specifically with JAM2-Fc. These characteristics of JAM2 led us to hypothesize a role for this novel protein in adhesion events associated with cardiac inflammatory conditions.

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“…Subsequently, Atherton and Born (3) developed the modern version of intravital microscopy and made the first quantitative observations of leukocyte rolling in the cheek pouch of hamsters and in mouse mesentery.…”

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confidence: 99%

Platelets roll on stimulated endothelium in vivo: an interaction mediated by endothelial P-selectin.

Frenette

Johnson

Hynes

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

428

289

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P-selectin, found in storage granules ofplatelets and endothelial cells, can be rapidly expressed upon stimulation. Mice lacking this membrane receptor exhibit a severe impairment of leukocyte rolling. We observed that, in addition to leukocytes, platelets were rolling in mesenteric venules of wild-typej mice. To investigate the role of P-selectin in this process, resting or activated platelets from wild-type or P-selectin-deficient mice were fluorescently labeled and transfused into recipients of either genotype. Platelet-endothelial interactions were monitored by intravital microscopy. We observed rolling of either wild-type or P-selectin-deficient resting platelets on wild-type endothelium. Endothelial stimulation with the calcium ionophore A23187 increased the number of platelets rolling 4-fold. Activated P-selectindeficient platelets behaved similarly, whereas activated wildtype platelets bound to leukocytes and were seen rolling together. Platelets of either genotype, resting or activated, interacted minimally with mutant endothelium even after A23187 treatment. The velocity of platelet rolling was 6-to 9-fold greater than that of leukocytes. Our results demonstrate that (i) platelets roll on endothelium in vivo, (ii) this interaction requires endothelial but not platelet P-selectin, and (iii) platelet rolling appears to be independent of platelet activation, indicating constitutive expression of a P-selectin ligand(s) on platelets. We have therefore observed an interesting parallel between platelets and leukocytes in that both of these blood cell types roll on stimulated vessel wall and that this process is dependent on the expression of endothelial P-selectin.Rolling of blood cells along the endothelial surface of venules was first described >150 years ago when leukocytes were shown to adhere to the walls of blood vessels and this interaction increased in inflammation (1, 2). Subsequently, Atherton and Born (3) developed the modern version of intravital microscopy and made the first quantitative observations of leukocyte rolling in the cheek pouch of hamsters and in mouse mesentery. Leukocyte rolling is the initial stage of a multistep process leading to extravasation of white blood cells to sites of inflammation or infection (4, 5). The selectin family has been shown by in vitro experimentation (6) and by intravital microscopy (7-9) to mediate this rolling motion.One member of this family of adhesion molecules, Pselectin, is stored preformed in a granules of platelets (10, 11) and in Weibel-Palade bodies of endothelial cells (12, 13). After stimulated secretion and expression on the cell surface, both platelet and endothelial P-selectin mediate adhesion to leukocytes (14, 15). Beside its role in binding to leukocytes, the biological relevance of platelet P-selectin, a specific marker of platelet activation, is still unknown. In vitro, neutrophils have been shown to roll on P-selectin of immobilized activated platelets (16). Endothelial P-selectin is a key mediator of leukocyte rolling and subseq...

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Quantitative investigations of the adhesiveness of circulating polymorphonuclear leucocytes to blood vessel walls

Cited by 351 publications

References 14 publications

Low Intensity Shear Stress Increases Endothelial ELR+ CXC Chemokine Production via a Focal Adhesion Kinase-p38β MAPK-NF-κB Pathway

Low Intensity Shear Stress Increases Endothelial ELR+ CXC Chemokine Production via a Focal Adhesion Kinase-p38β MAPK-NF-κB Pathway

A Novel Protein with Homology to the Junctional Adhesion Molecule

Platelets roll on stimulated endothelium in vivo: an interaction mediated by endothelial P-selectin.

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