Journal
MOLECULAR IMMUNOLOGY
Volume 46, Issue 3, Pages 406-415Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.molimm.2008.10.015
Keywords
Adhesion molecules; Endothelial cells; Human
Categories
Funding
- ZonMW [40-40600-98-06728]
- PPO-C [6-001]
- Landsteiner Foundation for Blood Transfusion Research [0112]
Ask authors/readers for more resources
Maternal human platelet antigen (HPA)-1a alloantibodies causing neonatal alloimmune thrombocytopenia can bind also to endothelium, via the beta 3-integrin (CD61). The aim of this study was to investigate the effect of HPA-1a Abs on endothelial cell function, with emphasis on monolayer integrity. We used a CD61 mAb as a model for the HPA-1a alloantibodies and confirmed the results With purified IgG fractions from HPA-1a alloimmunized women. The effect of these antibodies was examined by monitoring the adhesion, spreading, and monolayer integrity of primary HUVECs with conventional adhesion assays as well as electrical cell-substrate impedance sensing. We found that both the mAb CD61 and the HPAI a antibodies caused a significant reduction in HUVEC spreading. Moreover, addition of the mAb CD61 and the HPA-1a antibodies prior to or following formation of a stable endothelial monolayer negatively affected endothelial monolayer integrity, which was accompanied by a redistribution of junctional proteins. Our data suggest that HPA-1a alloantibodies have a direct effect on endothelial cell spreading and monolayer-integrity, which could contribute to the increased bleeding tendency in children with neonatal alloimmune thrombocytopenia. (C) 2008 Elsevier Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available