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Cellular and Molecular Aspects of Blood Cell–Endothelium Interactions in Vascular Disorders
In physiology and pathophysiology the molecules involved in blood cell–blood cell and blood cell–endothelium interactions have been identified. Platelet aggregation and adhesion to the walls belonging to vessels involve glycoproteins (GP), GP llb and GP llla and the GP Ib–IX–V complex. Red blood cel...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432596/ https://www.ncbi.nlm.nih.gov/pubmed/32727002 http://dx.doi.org/10.3390/ijms21155315 |
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author | Wautier, Jean-Luc Wautier, Marie-Paule |
author_facet | Wautier, Jean-Luc Wautier, Marie-Paule |
author_sort | Wautier, Jean-Luc |
collection | PubMed |
description | In physiology and pathophysiology the molecules involved in blood cell–blood cell and blood cell–endothelium interactions have been identified. Platelet aggregation and adhesion to the walls belonging to vessels involve glycoproteins (GP), GP llb and GP llla and the GP Ib–IX–V complex. Red blood cells (RBCs) in normal situations have little interaction with the endothelium. Abnormal adhesion of RBCs was first observed in sickle cell anemia involving vascular cell adhesion molecule (VCAM)-1, α4β1, Lu/BCAM, and intercellular adhesion molecule (ICAM)-4. More recently RBC adhesion was found to be increased in retinal-vein occlusion (RVO) and in polycythemia vera (PV). The molecules which participate in this process are phosphatidylserine and annexin V in RVO, and phosphorylated Lu/BCAM and α5 laminin chain in PV. The additional adhesion in diabetes mellitus occurs due to the glycated RBC band 3 and the advanced glycation end-product receptors. The multiligand receptor binds advanced glycation end products (AGEs) or S100 calgranulins, or β-amyloid peptide. This receptor for advanced glycation end products is known as RAGE. The binding to RAGE-activated endothelial cells leads to an inflammatory reaction and a prothrombotic state via NADPH activation and altered gene expression. RAGE blockade is a potential target for drugs preventing the deleterious consequences of RAGE activation. |
format | Online Article Text |
id | pubmed-7432596 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-74325962020-08-27 Cellular and Molecular Aspects of Blood Cell–Endothelium Interactions in Vascular Disorders Wautier, Jean-Luc Wautier, Marie-Paule Int J Mol Sci Review In physiology and pathophysiology the molecules involved in blood cell–blood cell and blood cell–endothelium interactions have been identified. Platelet aggregation and adhesion to the walls belonging to vessels involve glycoproteins (GP), GP llb and GP llla and the GP Ib–IX–V complex. Red blood cells (RBCs) in normal situations have little interaction with the endothelium. Abnormal adhesion of RBCs was first observed in sickle cell anemia involving vascular cell adhesion molecule (VCAM)-1, α4β1, Lu/BCAM, and intercellular adhesion molecule (ICAM)-4. More recently RBC adhesion was found to be increased in retinal-vein occlusion (RVO) and in polycythemia vera (PV). The molecules which participate in this process are phosphatidylserine and annexin V in RVO, and phosphorylated Lu/BCAM and α5 laminin chain in PV. The additional adhesion in diabetes mellitus occurs due to the glycated RBC band 3 and the advanced glycation end-product receptors. The multiligand receptor binds advanced glycation end products (AGEs) or S100 calgranulins, or β-amyloid peptide. This receptor for advanced glycation end products is known as RAGE. The binding to RAGE-activated endothelial cells leads to an inflammatory reaction and a prothrombotic state via NADPH activation and altered gene expression. RAGE blockade is a potential target for drugs preventing the deleterious consequences of RAGE activation. MDPI 2020-07-27 /pmc/articles/PMC7432596/ /pubmed/32727002 http://dx.doi.org/10.3390/ijms21155315 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Wautier, Jean-Luc Wautier, Marie-Paule Cellular and Molecular Aspects of Blood Cell–Endothelium Interactions in Vascular Disorders |
title | Cellular and Molecular Aspects of Blood Cell–Endothelium Interactions in Vascular Disorders |
title_full | Cellular and Molecular Aspects of Blood Cell–Endothelium Interactions in Vascular Disorders |
title_fullStr | Cellular and Molecular Aspects of Blood Cell–Endothelium Interactions in Vascular Disorders |
title_full_unstemmed | Cellular and Molecular Aspects of Blood Cell–Endothelium Interactions in Vascular Disorders |
title_short | Cellular and Molecular Aspects of Blood Cell–Endothelium Interactions in Vascular Disorders |
title_sort | cellular and molecular aspects of blood cell–endothelium interactions in vascular disorders |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7432596/ https://www.ncbi.nlm.nih.gov/pubmed/32727002 http://dx.doi.org/10.3390/ijms21155315 |
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