Shear Stress Affects Migration Behavior of Polymorphonuclear Cells Arrested on Endothelium

Kitayama, Joji; Hidemura, Akio; Saito, Hideaki; Nagawa, Hirokazu

doi:10.1006/cimm.2000.1671

Cited by 61 publications

(55 citation statements)

References 31 publications

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“…This observation is comparable with the reports that neutrophils moved more quickly and randomly once they transmigrated into the subendothelial layers. 11,27 The migration paths of transmigrated PBLs beneath the EC monolayers under disturbed flow were highly dependent on the flow direction, suggesting that the transmural flow and shear force can modulate PBL migration. The transmigrated PBLs showed the greatest stretch deformation and elongated with the flow direction in areas b and d, where the average shear stress is high (7 dyne/cm 2 ).…”

Section: Discussionmentioning

confidence: 99%

“…Weber et al 10 found that monocyte chemotactic protein-1 (MCP-1) and its receptor CCR2 mediate monocyte transmigration, which occurs under flow but rarely in stasis. Kitayama et al 11 showed that shear stress affects the transmigration of neutrophils arrested on ECs and that this is regulated by ␤1 integrins in the extracellular matrix. Cinamon et al 12,13 demonstrated that shear stress is essential for chemokineinduced transmigration of CD3 ϩ peripheral blood lymphocytes (PBLs) and that this involves signaling to lymphocyte-expressed G-protein-coupled receptors.…”

Section: Introductionmentioning

confidence: 99%

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Neutrophils, lymphocytes, and monocytes exhibit diverse behaviors in transendothelial and subendothelial migrations under coculture with smooth muscle cells in disturbed flow

Chen

Chang

Lee

et al. 2006

Blood

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neutrophils, lymphocytes, and monocytes exhibit diverse behaviors in transendothelial and subendothelial migrations under coculture with smooth muscle cells in disturbed flow

Chen

Chang

Lee

et al. 2006

Blood

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“…22,26,42 Although extravasation of neutrophils is known to be slightly faster under flow conditions, the molecules involved in this process are likely the same. 36,43 Real-time microscopy was used to dissect distinct molecular events governing neutrophil transendothelial migration. Because of their extreme brevity, these events are difficult to capture under fluid shear conditions.…”

Section: Discussionmentioning

confidence: 99%

CD157 plays a pivotal role in neutrophil transendothelial migration

Ortolan

Tibaldi

Ferranti

et al. 2006

Blood

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Paracellular diapedesis, a key step in leukocyte recruitment to the site of inflammation, occurs at endothelial junctions and is regulated by highly coordinated interactions between leukocytes and endothelium. We found that CD157, a glycosylphosphatidylinositol-anchored ectoenzyme belonging to the NADase/ADPribosyl cyclase family, plays a crucial role for neutrophil diapedesis, because its ligation with specific monoclonal antibodies (both on neutrophils or endothelial cells) results in altered neutrophil movement on the apical surface of endothelium and, ultimately, in loss of diapedesis. Realtime microscopy revealed that CD157 behaves as a sort of compass during the interaction between neutrophils and endothelial cells; indeed, following CD157 ligation, neutrophils appear disoriented, meandering toward junctions where they eventually stop without transmigrating. These findings are relevant in vivo because CD157-deficient neutrophils obtained from patients with paroxysmal nocturnal hemoglobinuria are characterized by a severely impaired diapedesis. IntroductionLeukocyte extravasation, a crucial step in immune responses and inflammatory reactions, is governed by sequential molecular interactions between leukocytes circulating in the bloodstream and endothelial cells lining the vascular wall. 1,2 This cascade involves initial tethering and rolling steps, prevalently mediated by selectinbased adhesive events 3 and a subsequent firm adhesion mediated by integrins. 4 Then, leukocytes polarize, move to endothelial cell junctions, and migrate through them in sequential processes referred to as locomotion and transendothelial migration (or diapedesis), respectively. 5,6 In contrast to leukocyte rolling and firm adhesion to endothelium, the molecular details of leukocyte diapedesis have not been completely defined. A small number of molecules have been identified that control the different steps of neutrophil and monocyte transendothelial migration; these include CD31, CD99, VE-cadherin, and junctional adhesion molecules (JAM-1, -2, and -3). [7][8][9][10] However, data derived from in vitro and in vivo models suggest that other molecules are involved in the process of diapedesis. 11,12 On molecular identification of these, several, unexpectedly, turned out to be ectoenzymes. 13 We addressed our attention to CD157 surface enzyme, a glycosylphosphatidylinositol (GPI)-linked molecule encoded by a member of the NADase/ ADP-ribosyl cyclase (cADPR) gene family, which also includes CD38. [14][15][16] The findings that CD157 is expressed both by neutrophils and endothelial cells and is implicated in neutrophil chemotaxis 17 were highly indicative of potential involvement in transendothelial migration and, eventually, in neutrophil recruitment to the inflammatory site.This work demonstrates that CD157 is (1) constitutively expressed at vascular interendothelial junctions and its expression is not affected by cell activation, (2) is crucial to transendothelial migration of neutrophils, and (3) orchestrates neutrophil journey thr...

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“…The integrin α6β1 is expressed by many cell types (Sonnenberg et al, 1988;Sonnenberg et al, 1987;Bohnsack, 1992;Terpe et al, 1994) including neutrophils, in which it is considered to be the major receptor for laminin. Studies in which mAbs against α6 integrins have blocked neutrophil migration through endothelial-cell monolayers cultured on laminin (Kitayama et al, 2000) or inhibited neutrophil migration through IL-1β-stimulated venules at the level of the PBM (Dangerfield et al, 2002) have strongly implicated integrin α6β1 in the process of leukocyte transmigration through the basement membrane. Another molecule implicated in this response is NE (Delclaux et al, 1996;Lee and Downey, 2001), a serine protease that has been shown to be mobilized to the leading edge of neutrophils migrating through cultured endothelial cells (Cepinskas et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

PECAM-1, α6 integrins and neutrophil elastase cooperate in mediating neutrophil transmigration

Wang

Dangerfield

Young

et al. 2005

Journal of Cell Science

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Shear Stress Affects Migration Behavior of Polymorphonuclear Cells Arrested on Endothelium

Cited by 61 publications

References 31 publications

Neutrophils, lymphocytes, and monocytes exhibit diverse behaviors in transendothelial and subendothelial migrations under coculture with smooth muscle cells in disturbed flow

Neutrophils, lymphocytes, and monocytes exhibit diverse behaviors in transendothelial and subendothelial migrations under coculture with smooth muscle cells in disturbed flow

CD157 plays a pivotal role in neutrophil transendothelial migration

PECAM-1, α6 integrins and neutrophil elastase cooperate in mediating neutrophil transmigration

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