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Cited by 42Hemoglobinopathies and Related DisordersBlood properties and coagulationCell Adhesion Molecules Research

Differential Expression of E‐ and P‐Selectin in the Microvasculature of Sickle Cell Transgenic Mice

Wood, Katherine, Russell, Janice, Hebbel, Robert P., Granger, D. Neil·2004·Microcirculation
DOI 10.1080/10739680490437559
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Abstract

Objective:There is a growing body of evidence that endothelial cells assume an inflammatory phenotype in sickle cell disease. The authors determined whether (1) the expression of E‐ and P‐selectin differs between sickle cell transgenic (β S) mice and their wild‐type counterparts, and (2) blood platelets and/or neutrophils contribute to the altered selectin expression. Methods:Expression of E‐ and P‐selectin was measured in different regional vascular beds of wild‐type and β S mice (with or without thrombocytopenia or neutropenia) using the dual radiolabeled monoclonal antibody technique. Results:Constitutive expression of P‐selectin was significantly increased in the heart, lungs, small bowel, large bowel, and penis of β S versus WT mice. While thrombocytopenia reduced P‐selectin expression in the small bowel and penis of β S mice, neutropenia was associated with a reduction in P‐selectin expression only in the penis. E‐selectin expression was not significantly elevated in any vascular bed except the penis of β S mice. Conclusions:Sickle cell disease promotes an increased P‐selectin expression in several vascular beds. An accumulation of platelets may explain the increased P‐selectin expression observed in some vascular beds.

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Crossref · 10.1080/10739680490437559

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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 [927]

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Authors
Wood, K., Russell, J., Hebbel, R. P., & Granger, D. N.
Affiliations
University of Minnesota (US)
Corresponding author
Granger, D. Neil
ORCID
Venue
Microcirculation
Publisher
Wiley
Published
2004-06
Volume
11
Issue
4
Pages
377-385
ISSN
  • 1073-9688 (ISSN-L)
  • 1549-8719
DOI
10.1080/10739680490437559
OpenAlex
W2154958048
Cited by
42
References
50
Citations by year
2023: 1 · 2022: 3 · 2021: 3 · 2020: 2 · 2019: 2 · 2018: 2 · 2016: 1 · 2015: 1 · 2014: 2 · 2013: 1 · 2012: 1
FWCI
2.76
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 2065 d)
Locations
  • Microcirculation (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p01hl055552-15)
  • National Heart, Lung, and Blood Institute (P01-HL055552, P01 HL55552)
  • National Institute of Diabetes and Digestive and Kidney Diseases (P01DK043785, DK-43785)
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, E-selectin, endothelial inflammation, microcirculation, thrombocytopenia, neutropenia, platelets, neutrophils, vascular bed
MeSH terms
Anemia, Sickle Cell, Animals, Endothelium, Vascular, Gene Expression Regulation, Globins, Humans, Inflammation, Mice, Transgenic, Microcirculation, Platelet Adhesiveness, Tissue Distribution, P-Selectin, E-Selectin, Mice

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