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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Online Access: | http://dx.doi.org/10.1155/2017/6138145 |
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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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