The Interaction of Selectins and PSGL-1 as a Key Component in Thrombus Formation and Cancer Progression

Cellular interaction is inevitable in the pathomechanism of human disease. Formation of heterotypic cellular aggregates, between distinct cells of hematopoietic and nonhematopoietic origin, may be involved in events leading to inflammation and the complex process of cancer progression. Among adhesio...

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Main Authors: János Kappelmayer, Béla Nagy
Format: Article
Language:English
Published: Hindawi Limited 2017-01-01
Series:BioMed Research International
Online Access:http://dx.doi.org/10.1155/2017/6138145
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spelling doaj-79e06d70ac824434893dfcb1aeb3f5ff2020-11-24T21:01:11ZengHindawi LimitedBioMed Research International2314-61332314-61412017-01-01201710.1155/2017/61381456138145The Interaction of Selectins and PSGL-1 as a Key Component in Thrombus Formation and Cancer ProgressionJános Kappelmayer0Béla Nagy1Department of Laboratory Medicine, Faculty of Medicine, University of Debrecen, Debrecen, HungaryDepartment of Laboratory Medicine, Faculty of Medicine, University of Debrecen, Debrecen, HungaryCellular interaction is inevitable in the pathomechanism of human disease. Formation of heterotypic cellular aggregates, between distinct cells of hematopoietic and nonhematopoietic origin, may be involved in events leading to inflammation and the complex process of cancer progression. Among adhesion receptors, the family of selectins with their ligands have been considered as one of the major contributors to cell-cell interactions. Consequently, the inhibition of the interplay between selectins and their ligands may have potential therapeutic benefits. In this review, we focus on the current evidence on the selectins as crucial modulators of inflammatory, thrombotic, and malignant disorders. Knowing that there is promiscuity in selectin binding, we outline the importance of a key protein that serves as a ligand for all selectins. This dimeric mucin, the P-selectin glycoprotein ligand 1 (PSGL-1), has emerged as a major player in inflammation, thrombus, and cancer development. We discuss the interaction of PSGL-1 with various selectins in physiological and pathological processes with particular emphasis on mechanisms that lead to severe disease.http://dx.doi.org/10.1155/2017/6138145
collection DOAJ
language English
format Article
sources DOAJ
author János Kappelmayer
Béla Nagy
spellingShingle János Kappelmayer
Béla Nagy
The Interaction of Selectins and PSGL-1 as a Key Component in Thrombus Formation and Cancer Progression
BioMed Research International
author_facet János Kappelmayer
Béla Nagy
author_sort János Kappelmayer
title The Interaction of Selectins and PSGL-1 as a Key Component in Thrombus Formation and Cancer Progression
title_short The Interaction of Selectins and PSGL-1 as a Key Component in Thrombus Formation and Cancer Progression
title_full The Interaction of Selectins and PSGL-1 as a Key Component in Thrombus Formation and Cancer Progression
title_fullStr The Interaction of Selectins and PSGL-1 as a Key Component in Thrombus Formation and Cancer Progression
title_full_unstemmed The Interaction of Selectins and PSGL-1 as a Key Component in Thrombus Formation and Cancer Progression
title_sort interaction of selectins and psgl-1 as a key component in thrombus formation and cancer progression
publisher Hindawi Limited
series BioMed Research International
issn 2314-6133
2314-6141
publishDate 2017-01-01
description Cellular interaction is inevitable in the pathomechanism of human disease. Formation of heterotypic cellular aggregates, between distinct cells of hematopoietic and nonhematopoietic origin, may be involved in events leading to inflammation and the complex process of cancer progression. Among adhesion receptors, the family of selectins with their ligands have been considered as one of the major contributors to cell-cell interactions. Consequently, the inhibition of the interplay between selectins and their ligands may have potential therapeutic benefits. In this review, we focus on the current evidence on the selectins as crucial modulators of inflammatory, thrombotic, and malignant disorders. Knowing that there is promiscuity in selectin binding, we outline the importance of a key protein that serves as a ligand for all selectins. This dimeric mucin, the P-selectin glycoprotein ligand 1 (PSGL-1), has emerged as a major player in inflammation, thrombus, and cancer development. We discuss the interaction of PSGL-1 with various selectins in physiological and pathological processes with particular emphasis on mechanisms that lead to severe disease.
url http://dx.doi.org/10.1155/2017/6138145
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