Role of CD11/CD18 in shear rate-dependent leukocyte-endothelial cell interactions in cat mesenteric venules.

Perry, Michael A.; Granger, D. Neil

doi:10.1172/jci115200

Cited by 239 publications

(120 citation statements)

References 19 publications

(16 reference statements)

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“…1). Following intraperitoneal glucose injection, shear force values were maintained in the physiological range (22), despite being significantly reduced (Table 1). These effects of hyperglycemia on venular shear rates are consistent with previous data showing comparable values in rat mesenteric venules following induction of experimental diabetes (23).…”

Section: Resultsmentioning

confidence: 99%

Mechanisms of Amelioration of Glucose-Induced Endothelial Dysfunction Following Inhibition of Protein Kinase C In Vivo

et al. 2002

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Section: Resultsmentioning

confidence: 99%

Mechanisms of Amelioration of Glucose-Induced Endothelial Dysfunction Following Inhibition of Protein Kinase C In Vivo

et al. 2002

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“…This shear was deemed below the physiologic shear that might be encountered in vivo. By contrast, 10 dynes/cm 2 would be approximately equivalent to 2 dynes/cm 2 in HBSS and would be encountered in the vasculature, as suggested from in vivo measurements [50].…”

Section: Flow Chamber Assaymentioning

confidence: 86%

Human fractalkine mediates leukocyte adhesion but not capture under physiological shear conditions; a mechanism for selective monocyte recruitment

et al. 2003

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Fractalkine is a unique chemokine possessing a long mucin-like stalk and a transmembrane region that has been proposed to act as an adhesion molecule. We investigated the ability of fractalkine to recruit leukocytes from whole blood, using an immobilized fractalkine fusion protein in the parallel-plate flow-chamber assay. Significant adhesion of leukocytes to fractalkine peaked at 2 dynes/cm 2 but was minimal at 10 dynes/cm 2 . In contrast, VCAM-1 could recruit cells from whole blood at 10 dynes/cm 2 . Co-immobilization of fractalkine and VCAM-1 at 10 dynes/cm 2 resulted in a twofold increase in adherent cells compared with VCAM-1 alone, suggesting that fractalkine can mediate adhesion at high shear if combined with a molecule that can mediate leukocyte tethering. Pretreatment of blood with pertussis toxin eliminated this increase in adhesion, implicating intracellular signaling in fractalkinemediated mechanisms of adhesion to co-immobilized fractalkine/VCAM-1. Analysis of the cell types recruited to fractalkine alone at low shear, or to fractalkine and VCAM-1 at 10 dynes/cm 2 , revealed that monocytes were recruited to fractalkine with the highest specificity. In conclusion, fractalkine is unlikely to act alone at shear forces found in most vascular beds where it most likely co-operates with tethering molecules, e.g. VCAM-1, in the recruitment of monocytes.

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“…The propensity for a leukocyte to undergo interactions with the endothelial surface is determined by the balance between proadhesive forces and the dispersive effects of the flowing blood, as evaluated by the microvascular shear rate (40). In both the LPS-treated and the TNF␣-treated mice, the microvascular shear rate was signifi- …”

Section: Discussionmentioning

confidence: 99%

Reduced leukocyte–endothelial cell interactions in the inflamed microcirculation of macrophage migration inhibitory factor–deficient mice

Gregory¹,

Leech²,

David³

et al. 2004

Arthritis & Rheumatism

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Objective. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine with established roles in a range of inflammatory conditions. However, it is not known whether MIF influences inflammation via the direct promotion of leukocyteendothelial cell interactions. Therefore, the aim of these experiments was to investigate the ability of MIF to regulate leukocyte-endothelial cell interactions in the inflamed microvasculature.Methods. Intravital microscopy was used to examine postcapillary venules in the cremaster muscle and synovium of wild-type and MIF ؊/؊ mice. Leukocyte-endothelial cell interactions (rolling, adhesion, emigration) were compared under a range of inflammatory conditions.Results. In cremasteric postcapillary venules of MIF ؊/؊ mice, lipopolysaccharide (LPS)-induced leukocyte rolling, adhesion, and emigration were significantly reduced relative to that in wild-type mice. Similar responses were observed in response to tumor necrosis factor ␣ and histamine. Examination of the synovial microvasculature following exposure to carrageenan revealed that leukocyte rolling and adhesion in synovial postcapillary venules and leukocyte entry into the joint space were also reduced significantly in MIF ؊/؊ mice. In each of these models, the level of P-selectindependent rolling was reduced in MIF ؊/؊ mice. Despite this, no difference in P-selectin expression was observed following LPS treatment. However, microvascular shear forces were elevated in MIF ؊/؊ mice, raising a possible mechanism to explain the reduced interactions in these animals.Conclusion. MIF ؊/؊ mice consistently displayed a reduction in P-selectin-dependent rolling, suggesting that MIF exerts proinflammatory effects, in part, via the promotion of P-selectin-mediated rolling. Together, these data indicate that MIF promotes interactions between leukocytes and endothelial cells, thereby enhancing the entry of leukocytes into sites of inflammation.

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Role of CD11/CD18 in shear rate-dependent leukocyte-endothelial cell interactions in cat mesenteric venules.

Abstract: In vivo microscopy was used to assess the relationships among shear rate (and shear

Cited by 239 publications

References 19 publications

Mechanisms of Amelioration of Glucose-Induced Endothelial Dysfunction Following Inhibition of Protein Kinase C In Vivo

Mechanisms of Amelioration of Glucose-Induced Endothelial Dysfunction Following Inhibition of Protein Kinase C In Vivo

Human fractalkine mediates leukocyte adhesion but not capture under physiological shear conditions; a mechanism for selective monocyte recruitment

Reduced leukocyte–endothelial cell interactions in the inflamed microcirculation of macrophage migration inhibitory factor–deficient mice

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