Microparticles from β-thalassaemia/HbE patients induce endothelial cell dysfunction
Abstract Thromboembolic complication occurs frequently in β-thalassaemia/HbE patients, particularly in splenectomised patients. Endothelial cells play an important role in thrombosis. There is strong evidence of endothelial cell activation and dysfunction in β-thalassaemia. Microparticles (MPs) are...
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2018
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oai:doaj.org-article:8ef7b6aa656b434a9cf31832e5054a982021-12-02T15:08:01ZMicroparticles from β-thalassaemia/HbE patients induce endothelial cell dysfunction10.1038/s41598-018-31386-62045-2322https://doaj.org/article/8ef7b6aa656b434a9cf31832e5054a982018-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-31386-6https://doaj.org/toc/2045-2322Abstract Thromboembolic complication occurs frequently in β-thalassaemia/HbE patients, particularly in splenectomised patients. Endothelial cells play an important role in thrombosis. There is strong evidence of endothelial cell activation and dysfunction in β-thalassaemia. Microparticles (MPs) are associated with thrombosis and endothelial cell dysfunction in many diseases including β-thalassaemia. However, the effect of thalassaemic-MPs on endothelial cells mediating thrombus formation has not been elucidated. In this study, the effects of circulating MPs from β-thalassaemia/HbE patients on endothelial cell functions were investigated. The results showed that MPs directly induce tissue factor, interleukin (IL)-6, IL-8, intracellular adhesion molecule-1, vascular cell adhesion molecule-1 and E-selectin expression in human umbilical vein endothelial cells (HUVECs). Notably, the levels of these endothelial cell activation markers were significantly increased in HUVECs treated with MPs obtained from splenectomised β-thalassaemia/HbE patients when compared to MPs from non-splenectomised patients or normal subjects. The increased endothelial cell activation ultimately lead to increased monocyte-endothelial cell adhesion. THP-1 and HUVECs adhesion induced by MPs from normal subjects, non-splenectomised and splenectomised patients increased to 2.0 ± 0.4, 2.3 ± 0.4 and 3.8 ± 0.4 fold, respectively when compared to untreated cells. This finding suggests that MPs play an important role on thrombosis and vascular dysfunction in β-thalassaemia/HbE disease, especially in splenectomised cases.Wasinee KheansaardKunwadee PhongpaoKittiphong PaiboonsukwongKovit PattanapanyasatPornthip ChaichompooSaovaros SvastiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-11 (2018) |
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Medicine R Science Q Wasinee Kheansaard Kunwadee Phongpao Kittiphong Paiboonsukwong Kovit Pattanapanyasat Pornthip Chaichompoo Saovaros Svasti Microparticles from β-thalassaemia/HbE patients induce endothelial cell dysfunction |
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Abstract Thromboembolic complication occurs frequently in β-thalassaemia/HbE patients, particularly in splenectomised patients. Endothelial cells play an important role in thrombosis. There is strong evidence of endothelial cell activation and dysfunction in β-thalassaemia. Microparticles (MPs) are associated with thrombosis and endothelial cell dysfunction in many diseases including β-thalassaemia. However, the effect of thalassaemic-MPs on endothelial cells mediating thrombus formation has not been elucidated. In this study, the effects of circulating MPs from β-thalassaemia/HbE patients on endothelial cell functions were investigated. The results showed that MPs directly induce tissue factor, interleukin (IL)-6, IL-8, intracellular adhesion molecule-1, vascular cell adhesion molecule-1 and E-selectin expression in human umbilical vein endothelial cells (HUVECs). Notably, the levels of these endothelial cell activation markers were significantly increased in HUVECs treated with MPs obtained from splenectomised β-thalassaemia/HbE patients when compared to MPs from non-splenectomised patients or normal subjects. The increased endothelial cell activation ultimately lead to increased monocyte-endothelial cell adhesion. THP-1 and HUVECs adhesion induced by MPs from normal subjects, non-splenectomised and splenectomised patients increased to 2.0 ± 0.4, 2.3 ± 0.4 and 3.8 ± 0.4 fold, respectively when compared to untreated cells. This finding suggests that MPs play an important role on thrombosis and vascular dysfunction in β-thalassaemia/HbE disease, especially in splenectomised cases. |
format |
article |
author |
Wasinee Kheansaard Kunwadee Phongpao Kittiphong Paiboonsukwong Kovit Pattanapanyasat Pornthip Chaichompoo Saovaros Svasti |
author_facet |
Wasinee Kheansaard Kunwadee Phongpao Kittiphong Paiboonsukwong Kovit Pattanapanyasat Pornthip Chaichompoo Saovaros Svasti |
author_sort |
Wasinee Kheansaard |
title |
Microparticles from β-thalassaemia/HbE patients induce endothelial cell dysfunction |
title_short |
Microparticles from β-thalassaemia/HbE patients induce endothelial cell dysfunction |
title_full |
Microparticles from β-thalassaemia/HbE patients induce endothelial cell dysfunction |
title_fullStr |
Microparticles from β-thalassaemia/HbE patients induce endothelial cell dysfunction |
title_full_unstemmed |
Microparticles from β-thalassaemia/HbE patients induce endothelial cell dysfunction |
title_sort |
microparticles from β-thalassaemia/hbe patients induce endothelial cell dysfunction |
publisher |
Nature Portfolio |
publishDate |
2018 |
url |
https://doaj.org/article/8ef7b6aa656b434a9cf31832e5054a98 |
work_keys_str_mv |
AT wasineekheansaard microparticlesfrombthalassaemiahbepatientsinduceendothelialcelldysfunction AT kunwadeephongpao microparticlesfrombthalassaemiahbepatientsinduceendothelialcelldysfunction AT kittiphongpaiboonsukwong microparticlesfrombthalassaemiahbepatientsinduceendothelialcelldysfunction AT kovitpattanapanyasat microparticlesfrombthalassaemiahbepatientsinduceendothelialcelldysfunction AT pornthipchaichompoo microparticlesfrombthalassaemiahbepatientsinduceendothelialcelldysfunction AT saovarossvasti microparticlesfrombthalassaemiahbepatientsinduceendothelialcelldysfunction |
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1718388330582769664 |