The contribution of endothelial cell P-selectin to the microvascular flow of mouse sickle erythrocytes in vivo

Embury, S. H.

doi:10.1182/blood-2004-02-0713

Cited by 141Hemoglobinopathies and Related DisordersBlood properties and coagulationCell Adhesion Molecules Research

The contribution of endothelial cell P-selectin to the microvascular flow of mouse sickle erythrocytes in vivo

Embury, S. H.·2004·Blood

DOI 10.1182/blood-2004-02-0713

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Abstract

Microvascular occlusion in sickle cell disease can be initiated by adhesion of sickle red blood cells (RBCs) to the endothelium. Our objective in this study was to verify the relevance in vivo of our discovery that sickle RBCs adhere abnormally to endothelial P-selectin in vitro. We used computer-assisted intravital microscopy to characterize RBC flow velocity (V(RBC)) in mice. We found faster V(RBC) of sickle RBCs in P-selectin knock-out and control mice than in sickle cell mice, which have increased endothelial cell P-selectin expression. Agonist peptide for murine protease-activated receptor-1 (PAR-1), which selectively activates mouse endothelial cells but not platelets, was used to assess the effects of endothelial cell P-selectin on microvascular flow. Suffusion of venules with this agonist stopped flow promptly in normal and sickle mice but not in P-selectin knock-out mice or in control mice pretreated with anti-P-selectin monoclonal antibody or unfractionated heparin (UFH). Agonist-induced slowing of flow was reversed rapidly by suffusion with UFH, provided flow had not already stopped. We conclude that endothelial cell P-selectin contributes to the microcirculatory abnormalities in sickle cell disease and that blocking P-selectin may be useful for preventing painful vasoocclusion in sickle cell disease.

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Selectins interact with sickled red cells and leukocytes in the circulation to facilitate endothelial adhesion and other interactions, ultimately contributing to vascular occlusion and sickle cell crisis.
“selectins interact with sickled red cells and leukocytes in the circulation to facilitate endothelial adhesion and other interactions (924 -927) ultimately contributing to vascular occlusion and ' sickle cell crisis ' (928).”
From Biological roles of glycans (2017) · cites this paper as [926]

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Short title: Endothelial P-selectin slows mouse sickle cell flow in vivo
Embury, S. H., Matsui, N. M., Mayadas, T. N., Noguchi, C. T., Diwan, B. A., & Mohandas, N. (2013)
Self-citation
Cellular Adhesion and the Endothelium
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A potent oral P‐selectin blocking agent improves microcirculatory blood flow and a marker of endothelial cell injury in patients with sickle cell disease
Kutlar, A., Ataga, K. I., McMahon, L. C., Howard, J., Galactéros, F., Hagar, W., Vichinsky, E. P., Cheung, A., Matsui, N. M., & Embury, S. H. (2012) · American Journal of Hematology · doi:10.1002/ajh.23147 · Cited by 76 · see citing works
Self-citation
The Nature of the P-Selectin Ligands on Sickle Cells.
Embury, S. H., Baran, C. E., Hefner, C. A., Seto, C. K., & Matsui, N. M. (2004) · Blood · doi:10.1182/blood.v104.11.363.363 · Cited by 2 · see citing works
Self-citation
P-selectin mediates the adhesion of sickle erythrocytes to the endothelium
Matsui, N. M., Borsig, L., Rosen, S. D., Yaghmai, M., Varki, A. P., & Embury, S. H. (2001) · Blood · doi:10.1182/blood.v98.6.1955 · Cited by 241 · see citing works
Self-citation

Authors: Embury, S. H.
Affiliations: Brigham and Women's Hospital (US)
Corresponding author: Embury, S. H.
Venue: Blood
Publisher: American Society of Hematology
Published: 2004-11-15
Volume: 104
Issue: 10
Pages: 3378-3385
ISSN: 0006-4971 (ISSN-L)
1528-0020
DOI: 10.1182/blood-2004-02-0713
OpenAlex: W1992525172
Cited by: 141
References: 75
Citations by year: 2026: 4 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 5 · 2021: 17 · 2020: 11 · 2019: 8 · 2018: 9 · 2017: 5 · 2016: 8 · 2015: 9 · 2014: 8 · 2013: 6 · 2012: 1
FWCI: 2.03
Type: journal article
Language: en
Open access: closed
Locations: Blood (publishedVersion, public-domain)
PubMed (publishedVersion)
Funders: National Institutes of Health (5p60hl020985-25, n01co12400-79-0-22, 5r01hl064396-03, 5r01hl067432-02)
University of California, Davis
National Heart, Lung, and Blood Institute (HL-31579, HL20985, R01HL031579, HL 64396, HL67432)
National Cancer Institute (N01CO12400)
Solar Energy Technologies Office
Topics: Health Sciences › Medicine › Genetics › Hemoglobinopathies and Related Disorders
Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Blood properties and coagulation
Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
Keywords: sickle cell disease, P-selectin, endothelial cells, sickle erythrocytes, microvascular blood flow, red blood cell adhesion, microvascular occlusion, protease-activated receptor 1, heparin, intravital microscopy
MeSH terms: Anemia, Sickle Cell, Animals, Antibodies, Monoclonal, Blood Flow Velocity, Cell Adhesion, Endothelium, Vascular, Erythrocytes, Heparin, Leukocytes, Mice, Inbred C57BL, Mice, Mutant Strains, Microcirculation, P-Selectin, Receptor, PAR-1, Mice

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The contribution of endothelial cell P-selectin to the microvascular flow of mouse sickle erythrocytes in vivo

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