TRAF3 negatively regulates platelet activation and thrombosis

Abstract CD40 ligand (CD40L), a member of the tumor necrosis factor (TNF) superfamily, binds to CD40, leading to many effects depending on target cell type. Platelets express CD40L and are a major source of soluble CD40L. CD40L has been shown to potentiate platelet activation and thrombus formation,...

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Autores principales:	Rui Zhang, Guoying Zhang, Binggang Xiang, Xiaofeng Chen, Lijang Tang, Shaojun Shi, Yani Liu, Xun Ai, Ping Xie, Zhenyu Li
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/542b33ec01f24af2b035a2a1c3fa2b1e
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spelling	oai:doaj.org-article:542b33ec01f24af2b035a2a1c3fa2b1e2021-12-02T15:06:24ZTRAF3 negatively regulates platelet activation and thrombosis10.1038/s41598-017-17189-12045-2322https://doaj.org/article/542b33ec01f24af2b035a2a1c3fa2b1e2017-12-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-17189-1https://doaj.org/toc/2045-2322Abstract CD40 ligand (CD40L), a member of the tumor necrosis factor (TNF) superfamily, binds to CD40, leading to many effects depending on target cell type. Platelets express CD40L and are a major source of soluble CD40L. CD40L has been shown to potentiate platelet activation and thrombus formation, involving both CD40-dependent and -independent mechanisms. A family of proteins called TNF receptor associated factors (TRAFs) plays key roles in mediating CD40L-CD40 signaling. Platelets express several TRAFs. It has been shown that TRAF2 plays a role in CD40L-mediated platelet activation. Here we show that platelet also express TRAF3, which plays a negative role in regulating platelet activation. Thrombin- or collagen-induced platelet aggregation and secretion are increased in TRAF3 knockout mice. The expression levels of collagen receptor GPVI and integrin αIIbβ3 in platelets were not affected by deletion of TRAF3, suggesting that increased platelet activation in the TRAF3 knockout mice was not due to increased expression platelet receptors. Time to formation of thrombi in a FeCl3-induced thrombosis model was significantly shortened in the TRAF3 knockout mice. However, mouse tail-bleeding times were not affected by deletion of TRAF3. Thus, TRAF3 plays a negative role in platelet activation and in thrombus formation in vivo.Rui ZhangGuoying ZhangBinggang XiangXiaofeng ChenLijang TangShaojun ShiYani LiuXun AiPing XieZhenyu LiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Rui Zhang Guoying Zhang Binggang Xiang Xiaofeng Chen Lijang Tang Shaojun Shi Yani Liu Xun Ai Ping Xie Zhenyu Li TRAF3 negatively regulates platelet activation and thrombosis
description	Abstract CD40 ligand (CD40L), a member of the tumor necrosis factor (TNF) superfamily, binds to CD40, leading to many effects depending on target cell type. Platelets express CD40L and are a major source of soluble CD40L. CD40L has been shown to potentiate platelet activation and thrombus formation, involving both CD40-dependent and -independent mechanisms. A family of proteins called TNF receptor associated factors (TRAFs) plays key roles in mediating CD40L-CD40 signaling. Platelets express several TRAFs. It has been shown that TRAF2 plays a role in CD40L-mediated platelet activation. Here we show that platelet also express TRAF3, which plays a negative role in regulating platelet activation. Thrombin- or collagen-induced platelet aggregation and secretion are increased in TRAF3 knockout mice. The expression levels of collagen receptor GPVI and integrin αIIbβ3 in platelets were not affected by deletion of TRAF3, suggesting that increased platelet activation in the TRAF3 knockout mice was not due to increased expression platelet receptors. Time to formation of thrombi in a FeCl3-induced thrombosis model was significantly shortened in the TRAF3 knockout mice. However, mouse tail-bleeding times were not affected by deletion of TRAF3. Thus, TRAF3 plays a negative role in platelet activation and in thrombus formation in vivo.
format	article
author	Rui Zhang Guoying Zhang Binggang Xiang Xiaofeng Chen Lijang Tang Shaojun Shi Yani Liu Xun Ai Ping Xie Zhenyu Li
author_facet	Rui Zhang Guoying Zhang Binggang Xiang Xiaofeng Chen Lijang Tang Shaojun Shi Yani Liu Xun Ai Ping Xie Zhenyu Li
author_sort	Rui Zhang
title	TRAF3 negatively regulates platelet activation and thrombosis
title_short	TRAF3 negatively regulates platelet activation and thrombosis
title_full	TRAF3 negatively regulates platelet activation and thrombosis
title_fullStr	TRAF3 negatively regulates platelet activation and thrombosis
title_full_unstemmed	TRAF3 negatively regulates platelet activation and thrombosis
title_sort	traf3 negatively regulates platelet activation and thrombosis
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/542b33ec01f24af2b035a2a1c3fa2b1e
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TRAF3 negatively regulates platelet activation and thrombosis

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