The Junctional Adhesion Molecule 3 (JAM-3) on Human Platelets is a Counterreceptor for the Leukocyte Integrin Mac-1

Santoso, Sentot; Sachs, Ulrich J.; Kroll, Hartmut; Linder, Monica; Ruf, Andreas; Preissner, Klaus T.; Chavakis, Triantafyllos

doi:10.1084/jem.20020267

Cited by 385 publications

(430 citation statements)

References 62 publications

(71 reference statements)

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“…JAM-1 has been described as a counter-receptor for CD11a/CD18 (Ostermann et al, 2002). Moreover, JAM-3, another novel counter receptor for CD11b/CD18 facilitates platelet-leukocyte interactions, and together with GPIba, appears to be the predominant counter-receptor for CD11b/ CD18 (Santoso et al, 2002). Analysis of different blood cell populations indicates that JAM-3 is exclusively expressed on platelets (Santoso et al, 2002).…”

Section: Leukocyte Recruitment and Activation: Influence Of Plateletsmentioning

confidence: 99%

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

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An alteration in the character and function of platelets is manifested in patients with inflammatory diseases, and these alterations have been dissociated from the well‐characterized involvement of platelets in thrombosis and haemostasis. Recent evidence reveals platelet activation is sometimes critical in the development of inflammation. The mechanisms by which platelets participate in inflammation are diverse, and offer numerous opportunities for future drug intervention. There is now acceptance that platelets act as innate inflammatory cells in immune responses, with roles as sentinel cells undergoing surveillance, responding to microbial invasion, orchestrating leukocyte recruitment, and migrating through tissue, causing damage and influencing repair processes in chronic disease. Some of these processes are targeted by drugs that are being developed to target platelet participation in atherosclerosis. The actions of platelets therefore influence the pathogenesis of diverse inflammatory diseases in various body compartments, encompassing parasitic and bacterial infection, allergic inflammation (especially asthma and rhinitis), and non‐atopic inflammatory conditions, for example, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and atherosclerosis. This review will first discuss the evidence for platelet activation in these various inflammatory diseases, and secondly discuss the mechanisms by which this pathogenesis occurs and the various anti‐platelet agents which have been developed to combat platelet activation in atherosclerosis and their potential future use for the treatment of other inflammatory diseases.British Journal of Pharmacology (2007) 152, 987–1002; doi:10.1038/sj.bjp.0707364; published online 2 July 2007

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Section: Leukocyte Recruitment and Activation: Influence Of Plateletsmentioning

confidence: 99%

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

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“…CD11b/ 18). Further adhesion partners of Mac-1 on the activated platelet cell membrane are GPIb [8] and Jam-3 [34]. Recently, Simon and his colleagues further identified aMI domain of Mac-1 as the binding site for platelet glycoprotein Iba and established the crucial role of GPIb-Mac-1 engagement for the biological response in vascular injury [35].…”

Section: Discussionmentioning

confidence: 99%

Involvement of platelet glycoprotein Ib in platelet microparticle mediated neutrophil activation

Hung

Lin

et al. 2006

J Biomed Sci

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SummaryPlatelet microparticles (MPs) are membrane vesicles shed by platelets after activation, and carry antigens characteristic of intact platelets, such as glycoprotein (GP) IIb/IIIa, GPIb and P-selectin. Elevated platelet MPs have been observed in many disorders in which platelet activation is documented. Recently, platelet GPIb has been implicated in the mediation of platelet-leukocyte interaction via binding to its ligand Mac-1 on leukocyte. The role of GPIb for mediating adhesion-activation interactions between platelet MPs and leukocytes has not been clarified. In this study we investigate the role of GPIb in the interplay between platelet MPs and neutrophils. Platelet MPs were obtained from collagen-stimulated platelet-rich plasma (PRP). In a study model of neutrophil aggregation, platelet MPs can serve a bridge to support neutrophil aggregation under venous level shear stress, suggesting that platelet MPs may enhance leukocyte aggregation, which would bear clinical relevance in diseases where the platelet MPs are elevated. The level of aggregation can be reduced by GPIb blocking antibodies, AP1 and SZ2, but not by anti-CD18 mAb. The GPIb blocking antibodies also decreased platelet MP-mediated neutrophil activation, including b2 integrin expression, adherence-dependent superoxide release and platelet MP-mediated neutrophil adherence to immobilized fibrinogen. Our data provide the evidence for the involvement of GPIb-Mac-1 interaction in the cross-talk between platelet MPs and neutrophils.

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“…It has previously been shown that JAM-C may not only mediate the migration of cells through EC junctions by providing an adhesive ligand for neutrophil Mac-1 but also regulate endothelia adherents junctions and barrier integrity. 6,7 This study therefore provides additional information to show that JAM-C may regulate the directionality of the migration of neutrophils through EC junctions in an abluminal-to-luminal direction.…”

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confidence: 81%