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Characterization of Sickling During Controlled Automated Deoxygenation with Oxygen Gradient Ektacytometry

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Role of erythrocyte phosphatidylserine in sickle red cell-endothelial adhesion.

B N Yamaja Setty¹, Surekha Kulkarni, Marie J Stuart

¹Division of Research Hematology, Department of Pediatrics, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA. yamaja.setty@mail.tju.edu

|February 28, 2002

Summary

Phosphatidylserine (PS) exposure on red blood cells significantly increases adhesion in sickle cell disease (SCD). This PS exposure is a primary driver of sickle erythrocyte adhesion, more so than CD36, impacting vascular pathology.

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Published on: November 29, 2024

Area of Science:

Hematology
Cell Biology
Vascular Biology

Background:

Sickle cell disease (SCD) is characterized by erythrocyte membrane instability.
Phosphatidylserine (PS) exposure on the erythrocyte surface promotes adhesion to the vascular endothelium.
The role of PS in sickle erythrocyte-microendothelial adhesion requires further elucidation.

Purpose of the Study:

To assess the contribution of phosphatidylserine (PS) exposure to sickle erythrocyte-microendothelial adhesion.
To compare the adhesion-promoting role of PS with the known receptor CD36 in SCD.
To investigate the correlation between PS levels and adhesion in SCD patients.

Main Methods:

Plasma-induced adhesion assays were performed on unactivated endothelium.
Erythrocytes were treated with annexin V (to block PS) or anti-CD36 antibodies.
Erythrocyte adhesion markers (PS and CD36) were quantified in 87 SCD patient blood samples.

Main Results:

Blocking PS significantly inhibited sickle erythrocyte adhesion (36% +/- 10%), while blocking CD36 had a lesser effect (23% +/- 8%).
Blocking both PS and CD36 suggested an additive inhibitory effect on adhesion.
A strong positive correlation was found between erythrocyte PS positivity and adhesion in SCD patients (R = 0.52, P <.000 001).
No significant correlation was observed between adhesion and CD36 levels (R = 0.2, P >.07).
PS was identified as the predominant adhesion marker compared to CD36, particularly on stress reticulocytes.

Conclusions:

Erythrocyte phosphatidylserine (PS) exposure is a significant contributor to sickle erythrocyte-microendothelial adhesion in SCD.
PS is a more critical adhesion marker than CD36 in the context of SCD vascular pathology.
Further assessment of PS exposure's implications in SCD vascular pathology is warranted.