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Cho, Ko, Cheon, Jeoung, Kim, and Choe: Platelets Induce Proliferation of Human Umbilical Vein Endothelial Cells via CD154-CD40 Pathway Independently of VEGF
Original Article

Immune Network 2008; 8(3): 75-81.

Published online: 30 September 2008

DOI: https://doi.org/10.4110/in.2008.8.3.75

Platelets Induce Proliferation of Human Umbilical Vein Endothelial Cells via CD154-CD40 Pathway Independently of VEGF

Whajung Cho1, 2, Eun-Mi Ko1, 2, In Su Cheon1, 2, Doo-Il Jeoung2, Young-Myeong Kim2, Jongseon Choe1, 2

1Department of Microbiology and Immunology, College of Medicine, Kangwon National University, Chuncheon, Korea.

2Vascular System Research Center, Kangwon National University, Chuncheon, Korea.

Corresponding Author. Tel: 82-33-250-8862; Fax: 82-33-242-7571; jchoe@kangwon.ac.kr

Received 4 August 2008       Revised 14 August 2008       Accepted 21 August 2008

Copyright © 2008 The Korean Association of Immunologists

(open-access):

This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background

Platelets take part in repairing the lesions of endothelial damage. To understand the molecular mechanism of this process, we tested the hypothesis that CD154 expressed on activated platelets stimulates proliferation of human endothelial cells.

Methods

The expression levels of CD154 and CD40 on platelets and endothelial cells, respectively, were measured by flow cytometry and confocal microscopy. Function-blocking monoclonal antibody against CD154 was developed after immunization with CD154-transfected L cells.

Results

An anti-CD40 agonist antibody and soluble CD154 both induced significant proliferation of endothelial cells. In addition, a function-blocking anti-CD154 antibody inhibited the platelet-induced proliferation of endothelial cells, indicating that the CD154-CD40 pathway is involved in these cellular interactions. An anti-VEGF antibody failed to inhibit the proliferation. This, in addition to the fact that very small amounts of VEGF are released from platelets or endothelial cells, suggests that VEGF does not play an important role in the platelet-stimulated proliferation of endothelial cells.

Conclusion

Our results indicate that platelets induce proliferation of endothelial cells by CD154-CD40 interactions independently of VEGF.

Keywords: platelet, HUVEC, proliferation, CD40, CD154, VEGF

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