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Citations to this article

Abnormal Adherence of Sickle Erythrocytes to Cultured Vascular Endothelium: POSSIBLE MECHANISM FOR MICROVASCULAR OCCLUSION IN SICKLE CELL DISEASE
Robert P. Hebbel, … , James G. White, John W. Eaton
Robert P. Hebbel, … , James G. White, John W. Eaton
Published January 1, 1980
Citation Information: J Clin Invest. 1980;65(1):154-160. https://doi.org/10.1172/JCI109646.
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Article has an altmetric score of 6

Abnormal Adherence of Sickle Erythrocytes to Cultured Vascular Endothelium: POSSIBLE MECHANISM FOR MICROVASCULAR OCCLUSION IN SICKLE CELL DISEASE

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Abstract

The abnormal shape and poor deformability of the sickled erythrocyte (RBC) have generally been held responsible for the microvascular occlusions of sickle cell disease. However, there is no correlation between the clinical severity of this disease and the presence of sickled RBC. In searching for additional factors that might contribute to the pathophysiology of sickle cell disease, we have investigated the possibility that sickle RBC might be less than normally repulsive of the vascular endothelium. After RBC suspensions are allowed to settle onto plates of cultured human endothelial cells, normal RBC are completely removed by as few as six washes. In contrast, sickle RBC remain adherent despite multiple washes. On subconfluent culture plates, normal RBC are distributed randomly, whereas sickle RBC cluster around endothelial cells. Sickle RBC adherence is not enhanced by deoxygenation but does increase with increasing RBC density. The enzymatic removal of membrane sialic acid greatly diminishes the adherence of sickle RBC to endothelial cells, suggesting that sialic acid participates in this abnormal cell-cell interaction. Although net negative charge appears normal, sickle RBC mainfest an abnormal clumping of negative surface charge as demonstrated by localization of cationized ferritin. These abnormalities are reproduced in normal RBC loaded with nonechinocytogenic amounts of calcium. We conclude that sickle RBC adhere to vascular endothelial cells in vitro, perhaps caused by a calcium-induced aberration of membrane topography. This adherence may be a pathogenetic factor in the microvascular occlusions characteristic of sickle cell disease.

Authors

Robert P. Hebbel, Osamu Yamada, Charles F. Moldow, Harry S. Jacob, James G. White, John W. Eaton

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Citations: 1 2 4 5 3 7 7 10 7 15 7 10 2 5 4 10 8 9 5 5 3 5 7 7 7 8 6 6 7 6 2 6 7 4 7 7 2 13 10 16 7 6 4 6 1 1 1 1 289
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Citations to this article in year 2012 (5)

Title and authors Publication Year
Effect of Propranolol as Anti-Adhesive Therapy in Sickle Cell Disease
LM de Castro, R Zennadi, JC Jonassaint, M Batchvarova, MJ Telen
Clinical and Translational Science 2012
A novel hemoglobin-binding peptide reduces cell-free hemoglobin in murine hemolytic anemia
MS Hanson, H Xu, TC Flewelen, SL Holzhauer, D Retherford, DW Jones, AC Frei, KA Pritchard, CA Hillery, N Hogg, NJ Wandersee
American journal of physiology. Heart and circulatory physiology 2012
Massively Parallel Single-Molecule and Single-Cell Emulsion Reverse Transcription Polymerase Chain Reaction Using Agarose Droplet Microfluidics
H Zhang, G Jenkins, Y Zou, Z Zhu, CJ Yang
Analytical Chemistry 2012
Design, Synthesis, and Pharmacological Evaluation of Novel Hybrid Compounds to Treat Sickle Cell Disease Symptoms. Part II: Furoxan Derivatives
JL Santos, C Lanaro, RC Chelucci, S Gambero, PL Bosquesi, JS Reis, LM Lima, H Cerecetto, M González, FF Costa, MC Chung
Journal of Medicinal Chemistry 2012
ACSM and CHAMP Summit on Sickle Cell Trait: Mitigating Risks for Warfighters and Athletes
FG O’connor, MF Bergeron, J Cantrell, P Connes, KG Harmon, E Ivy, J Kark, D Klossner, P Lisman, BK Meyers, K O’brien, K Ohene-Frempong, AA Thompson, J Whitehead, PA Deuster
Medicine and Science in Sports and Exercise 2012

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