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Circulating extracellular vesicles from patients with traumatic brain injury induce cerebrovascular endothelial dysfunction

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WOS体系：
Pubmed体系：

收录情况： ◇ SCIE

作者：
Li Lei[1,2,3] * ; Li Fanjian[2,3] * ; Bai Xuesong[1,4] ; Jia Haoran[2,3] ; Wang Cong[2,3] ; Li Peng[1,5] ; Zhang Qiaoling[2,3] ; Guan Siyu[2,3] ; Peng Ruilong[2,3] ; Zhang Shu[2,3] ; Dong Jing-Fei[6] ; Zhang Jianning[2,3,*1] ; Xu Xin[1,4,*2] ;
机构： [1]Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, 45 Changchun Street, Beijing, China [2]Department of Neurosurgery, Tianjin Medical University General Hospital, 154 Anshan Road, Tianjin, China [3]Tianjin Neurological Institute, Tianjin Medical University General Hospital, 154 Anshan Road, Tianjin, China [4]China International Neuroscience Institute (China-INI), 45 Changchun Street, Beijing, China [5]Department of Neurosurgery, Beijing Fengtai You’anmen Hospital, 199 You’anmen Outer Street, Beijing, China [6]Bloodworks Research Institute and Division of Hematology, Department of Medicine, University of Washington, School of Medicine, Seattle, WA, USA
出处：
DOI： 10.1016/j.phrs.2023.106791
ISSN：

关键词： Traumatic brain injury Endothelial cell dysfunction Extracellular vesicles High mobility group box 1 Von Willebrand factor

摘要：
Endothelial dysfunction is a key proponent of pathophysiological process of traumatic brain injury (TBI). We previously demonstrated that extracellular vesicles (EVs) released from injured brains led to endothelial barrier disruption and vascular leakage. However, the molecular mechanisms of this EV-induced endothelial dysfunction (endotheliopathy) remain unclear. Here, we enriched plasma EVs from TBI patients (TEVs), and detected high mobility group box 1 (HMGB1) exposure to 50.33 ± 10.17% of TEVs and the number of HMGB1+TEVs correlated with injury severity. We then investigated for the first time the impact of TEVs on endothelial function using adoptive transfer models. We found that TEVs induced dysfunction of cultured human umbilical vein endothelial cells and mediated endothelial dysfunction in both normal and TBI mice, which were propagated through the HMGB1-activated receptor for advanced glycation end products (RAGE)/Cathepsin B signaling, and the resultant NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation and canonical caspase-1/gasdermin D (GSDMD)-dependent pyroptosis. Finally, von Willebrand factor (VWF) was detected on the surface of 77.01 ± 7.51% of HMGB1+TEVs. The TEV-mediated endotheliopathy was reversed by a polyclonal VWF antibody, indicating that VWF might serve a coupling factor that tethered TEVs to ECs, thus facilitating HMGB1-induced endotheliopathy. These results suggest that circulating EVs isolated from patients with TBI alone are sufficient to induce endothelial dysfunction and contribute to secondary brain injury that are dependent on immunologically active HMGB1 exposed on their surface. This finding provided new insight for the development of potential therapeutic targets and diagnostic biomarkers for TBI.Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.

基金：
National Natural Science Foundation of China (grant 82001317, 81930031, 81901525, and 81720108015) and the Beijing Hospitals Authority Youth Programme (grant QML20230801).
语种：
外文
被引次数：
WOS：
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中科院(CAS)分区：
出版当年[2022]版：
大类 | 1 区 医学
小类 | 1 区 药学
最新[2025]版：
大类 | 2 区 医学
小类 | 1 区 药学
JCR分区：
出版当年[2021]版：
Q1 PHARMACOLOGY & PHARMACY
最新[2023]版：
Q1 PHARMACOLOGY & PHARMACY

影响因子： 最新[2023版] 最新五年平均 出版当年[2021版] 出版当年五年平均 出版前一年[2020版] 出版后一年[2022版]

第一作者：
第一作者机构： [1]Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, 45 Changchun Street, Beijing, China [2]Department of Neurosurgery, Tianjin Medical University General Hospital, 154 Anshan Road, Tianjin, China [3]Tianjin Neurological Institute, Tianjin Medical University General Hospital, 154 Anshan Road, Tianjin, China
共同第一作者：
通讯作者：
通讯机构： [1]Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, 45 Changchun Street, Beijing, China [2]Department of Neurosurgery, Tianjin Medical University General Hospital, 154 Anshan Road, Tianjin, China [3]Tianjin Neurological Institute, Tianjin Medical University General Hospital, 154 Anshan Road, Tianjin, China [4]China International Neuroscience Institute (China-INI), 45 Changchun Street, Beijing, China [*1]Department of Neurosurgery, Tianjin Medical University General Hospital, 154 Anshan Road, 300052, Tianjin, China. [*2]Department of N eurosurgery, Xuanwu Hospital, Capital Medical University, 45 Changchun Street, Beijing 100053, China.
推荐引用方式(GB/T 7714)：
Li Lei,Li Fanjian,Bai Xuesong,et al.Circulating extracellular vesicles from patients with traumatic brain injury induce cerebrovascular endothelial dysfunction[J].PHARMACOLOGICAL RESEARCH.2023,192:doi:10.1016/j.phrs.2023.106791.
APA：
Li Lei,Li Fanjian,Bai Xuesong,Jia Haoran,Wang Cong...&Xu Xin.(2023).Circulating extracellular vesicles from patients with traumatic brain injury induce cerebrovascular endothelial dysfunction.PHARMACOLOGICAL RESEARCH,192,
MLA：
Li Lei,et al."Circulating extracellular vesicles from patients with traumatic brain injury induce cerebrovascular endothelial dysfunction".PHARMACOLOGICAL RESEARCH 192.(2023)

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