P-selectin and MAC-1 mediate monocyte rolling and adhesion to ECM-bound platelets under flow conditions

Kuijper, P. H. M.; Torres, H. I. Gallardo; Houben, L. A. M. J.; Lammers, Jan-Willem; Zwaginga, Jaap Jan; Koenderman, Leo

doi:10.1002/jlb.64.4.467

Cited by 60 publications

(54 citation statements)

References 45 publications

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“…Similar results were found on atherosclerotic endothelium (25), on which VCAM-1 is also highly expressed. In an in vitro model of monocyte adhesion to the injured vessel wall, Kuijper et al (26) found that Mac-1 is the predominant integrin mediating monocyte rolling on ECM alone and that the interaction of PSGL-1 with P-selectin as well as Mac-1 accounts for nearly all the rolling interactions on activated platelets bound to ECM substrates at low shear stress.…”

Section: Leukocyte Recruitmentmentioning

confidence: 99%

Integrin Regulation during Leukocyte Recruitment

Herter

Zarbock

2013

The Journal of Immunology

170

138

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Integrins are recognized as vital players in leukocyte recruitment. Integrin malfunction causes severe disease patterns characterized by the inability to fight pathogens. Although inflammatory reactions are beneficial and necessary for host defense, these reactions have to be controlled to prevent tissue destruction and harmful sequelae. In this review, we discuss the different signaling pathways leading to the change of integrin adhesiveness in neutrophils, monocytes, and lymphocytes. We thereby focus on the importance of integrin activation for the different steps of the leukocyte recruitment cascade, including rolling, adhesion, postadhesion strengthening, intravascular crawling, and transmigration, as each step necessitates the proper functioning of a distinct set of integrin molecules that has to be activated specifically. Additionally, we discuss endogenous mechanisms that balance and counteract integrin activation and limit leukocyte recruitment at the site of inflammation. Further insight into these complex mechanisms may provide new approaches for developing new anti-inflammatory therapies.

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Section: Leukocyte Recruitmentmentioning

confidence: 99%

Integrin Regulation during Leukocyte Recruitment

Herter

Zarbock

2013

The Journal of Immunology

170

138

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“…[1][2][3] After endothelial denudation, exposure of the basement membrane and subendothelial matrix leads to the deposition of fibrin and adherent platelets, which on activation and degranulation express P-selectin and present fibrinogen, thereby mediating leukocyte rolling and arrest, and supporting their inflammatory recruitment. 4,5 Because of secretion of cytokines or growth factors, monocyte-derived macrophages may be associated with lesion progression, including the proliferation of migrated smooth muscle cells. 2 The increase in neointima is accompanied by a reendothelialization, which is usually completed after 3 weeks.…”

mentioning

confidence: 99%

Deposition of Platelet RANTES Triggering Monocyte Recruitment Requires P-Selectin and Is Involved in Neointima Formation After Arterial Injury

et al. 2002

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Background-Chemokines expressed on atherosclerotic endothelium or deposited by activated platelets have been implicated in monocyte recruitment during atherogenesis and restenosis. Although the involvement of P-selectin in these processes is evident from studies in knockout mice, it has not been elucidated whether delivery of platelet chemokines requires P-selectin, thus serving as a P-selectin-dependent effector function. Methods and Results-Using immunofluorescence and laminar flow assays, we found that the deposition of the platelet-derived chemokine RANTES and monocyte arrest subsequently triggered by RANTES immobilized on inflamed endothelium are more efficient after preperfusion than after static preincubation of platelets and appear to depend on interactions of platelet but not endothelial P-selectin. This was revealed by the effects of P-selectin antibodies and comparison of P-selectin-deficient and wild-type platelets. Immunohistochemistry detected a substantial luminal expression of RANTES on neointimal lesions in wire-injured carotid arteries of apolipoprotein E (apoE)-deficient mice but not of mice with a combined deficiency in apoE and P-selectin (or platelet P-selectin). As assessed by histomorphometry, treatment of apoE-deficient mice with the RANTES receptor antagonist Met-RANTES markedly reduced neointimal plaque area and macrophage infiltration. Conclusions-Our data suggest that RANTES deposition and subsequent monocyte arrest are promoted by platelet P-selectin and involved in wire-induced intimal hyperplasia, and that blocking RANTES receptors attenuates neointima formation and macrophage infiltration. This mechanism represents an important component explaining the protection against neointimal growth in P-selectin-deficient mice and may represent a novel approach to the treatment of restenosis or atherosclerosis by the administration of chemokine receptor antagonists.

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“…In accordance, we found a comparable effect of platelet coverage on monocyte adhesion. 24 More platelets and thus P-selectin presence only lowers rolling velocity. Lawrence et al 25 reported a similar decrease in rolling velocity when more purified P-selectin was coated on coverslips.…”

Section: Discussionmentioning

confidence: 99%

Minimal Platelet Deposition and Activation in Models of Injured Vessel Wall Ensure Optimal Neutrophil Adhesion Under Flow Conditions

Zwaginga

Torres

Lammers

et al. 1999

ATVB

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Abstract-Platelets at injured vessel wall form an adhesive surface for leukocyte adhesion. The precise relation between platelet adhesion and activation and leukocyte adhesion, however, is not known. We therefore used various models of injured vessel wall to form different patterns of platelet adhesion. The interaction of polymorphonuclear neutrophils (PMNs) was subsequently studied under flow conditions. In the absence of platelets, not only endothelial cell, smooth muscle cell, and fibroblast matrices but also purified matrix proteins (fibrinogen, collagen, and fibronectin) barely support PMN adhesion. The presence of platelets, however, strongly enhances PMN adhesion. PMN adhesion shows a proportional increase with platelet coverage up to 15%. Although PMNs roll over the scarcely scattered platelets, they speed up again when encountering surfaces without platelets. This "hopping" interaction of PMNs vanishes with platelet coverage Ͼ15%. Unobstructed rolling of PMNs is than observed and soon leads to a maximal adhesion of 1000 to 1200 cells/mm 2 . The mean rolling velocity of PMNs continues to decrease with higher platelet coverage. Platelet aggregate formation is an accepted indicator of platelet activation. The presence of platelet aggregates instead of contact or spread platelets, however, does not increase PMN adhesion. Also, additional stimulation of surface-associated platelets by thrombin fails to influence PMN adhesion. Moreover, indomethacin as an inhibitor of platelet activation and aggregation does not change the subsequent PMN interaction. In conclusion, approximately 15% of platelet coverage is sufficient for optimal PMN adhesion. Increasing platelet coverage increases the availability of platelet-associated receptors that lower PMN rolling velocity. Additional activation of adherent platelets makes no difference in the expression of relevant adhesion receptors. Therefore, minimal vascular damage in vivo and only scarce platelet adhesion will already evoke significant colocalization of leukocytes. Key Words: platelet adhesiveness Ⅲ thrombosis pathophysiology Ⅲ vascular injury Ⅲ leukocyte adhesion Ⅲ flow P latelet adhesion at the injured vessel wall was convincingly shown to support leukocyte adhesion under flow conditions. 1-3 The observed colocalization of the hemostatic and inflammatory response in thrombosis, vasculitis, and atherosclerosis in vivo supports the role of these interactions in pathophysiology of these diseases. 4 -6 Recent research both in vivo and in vitro in perfusion chambers showed that platelets at the injured vessel wall form an extremely powerful substrate for leukocyte, eg, polymorphonuclear neutrophil (PMN) adhesion under flow conditions. The first step in PMN adhesion consists of a rolling or tethering interaction involving P-selectin 1-3 expressed by activated platelets and P-selectin glycoprotein ligand-1 by leukocytes. Firm adhesion follows by integrin-ligand interactions. Mac-1 (CD11bCD18) was identified to be the main leukocyte ␤2 integrin that binds to the platele...

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P-selectin and MAC-1 mediate monocyte rolling and adhesion to ECM-bound platelets under flow conditions

Cited by 60 publications

References 45 publications

Integrin Regulation during Leukocyte Recruitment

Integrin Regulation during Leukocyte Recruitment

Deposition of Platelet RANTES Triggering Monocyte Recruitment Requires P-Selectin and Is Involved in Neointima Formation After Arterial Injury

Minimal Platelet Deposition and Activation in Models of Injured Vessel Wall Ensure Optimal Neutrophil Adhesion Under Flow Conditions

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