Vitamin E induces phosphatidylserine externalization and red cell adhesion to endothelial cells

Alexander Koshkaryev; Gregory Barshtein; Saul Yedgar

doi:10.1007/s12013-009-9074-3

Vitamin E induces phosphatidylserine externalization and red cell adhesion to endothelial cells

Alexander Koshkaryev, Gregory Barshtein^*, Saul Yedgar

^*Corresponding author for this work

Department of Biochemistry and Molecular Biology

Research output: Contribution to journal › Article › peer-review

4 Scopus citations

Abstract

Red blood cell (RBC) adhesion to vessel wall endothelium is a potent catalyst of vascular occlusion and occurs in oxidative stress states such as hemoglobinopathies and cardiovascular conditions. These are often treated with vitamin E (VitE), a "classic" antioxidant. In this study, we examined the effects of VitE on RBC adhesion to vascular endothelial cells (EC), and on translocation of phosphatidylserine (PS) to RBC surface, known as a potent mediator of RBC/EC adhesion, facilitating thrombus formation. Treatment of RBC with VitE strongly induces (up to sevenfold) PS externalization and enhances (up to 20-fold) their adherence to EC. The VitE hydrophilic analogue-Trolox-does not incorporate into cell membranes. Trolox did not exhibit any of these effects, implying that the VitE effect is due to its known ability to incorporate into cell membranes. The membrane-incorporated VitE significantly reduced the level of reactive oxygen species in H₂O₂-treated RBC, demonstrating that VitE elevates RBC/EC adhesion despite acting as an anti-oxidant. This study demonstrates for the first time that contrary to the common view of VitE as a beneficial supplement, VitE may introduce a circulatory risk by inducing flow-disturbing RBC adherence to blood vessel wall and the pro-thrombotic PS exposure.

Original language	English
Pages (from-to)	109-114
Number of pages	6
Journal	Cell Biochemistry and Biophysics
Volume	56
Issue number	2
DOIs	https://doi.org/10.1007/s12013-009-9074-3
State	Published - Apr 2010

Bibliographical note

Funding Information:
Acknowledgments This study was supported by grants from the US National Blood Foundation (American Association of Blood Banking, to S.Y. and G.B.), the Israel Ministry of Health (to S.Y.), the Israel Science Foundation (No. 558/03 to S.Y. and G.B.), the US-Israel BSF (to S.Y. and G.B.), and the Walter and Greta Stiel Chair for Heart Studies (S.Y.). The authors thank Mrs. O. Fredman for her technical assistance.

Keywords

Adherence
Endothelial cells
Phosphatidylserine
Red blood cells
α-Tocopherol

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10.1007/s12013-009-9074-3

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abstract = "Red blood cell (RBC) adhesion to vessel wall endothelium is a potent catalyst of vascular occlusion and occurs in oxidative stress states such as hemoglobinopathies and cardiovascular conditions. These are often treated with vitamin E (VitE), a {"}classic{"} antioxidant. In this study, we examined the effects of VitE on RBC adhesion to vascular endothelial cells (EC), and on translocation of phosphatidylserine (PS) to RBC surface, known as a potent mediator of RBC/EC adhesion, facilitating thrombus formation. Treatment of RBC with VitE strongly induces (up to sevenfold) PS externalization and enhances (up to 20-fold) their adherence to EC. The VitE hydrophilic analogue-Trolox-does not incorporate into cell membranes. Trolox did not exhibit any of these effects, implying that the VitE effect is due to its known ability to incorporate into cell membranes. The membrane-incorporated VitE significantly reduced the level of reactive oxygen species in H2O2-treated RBC, demonstrating that VitE elevates RBC/EC adhesion despite acting as an anti-oxidant. This study demonstrates for the first time that contrary to the common view of VitE as a beneficial supplement, VitE may introduce a circulatory risk by inducing flow-disturbing RBC adherence to blood vessel wall and the pro-thrombotic PS exposure.",

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author = "Alexander Koshkaryev and Gregory Barshtein and Saul Yedgar",

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Vitamin E induces phosphatidylserine externalization and red cell adhesion to endothelial cells

Abstract

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Keywords

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