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Brain-derived extracellular vesicles mediate systemic coagulopathy and inflammation after traumatic brain injury

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机构: [1]Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, China [2]Tianjin Neurological Institute, Tianjin, China [3]Graduate School, Tianjin Medical University, Tianjin, China [4]Key Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous System, Ministry of Education, Tianjin, China [5]Tianjin Key Laboratory of Injuries, Variations and Regeneration of Nervous System, Tianjin, China [6]Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, 45 Changchun Street, Beijing, China
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关键词: Traumatic brain injury Extracellular vesicles Coagulopathy Inflammation Lactadherin

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Traumatic brain injury (TBI) can induce systemic coagulopathy and inflammation, thereby increasing the risk of mortality and disability. However, the mechanism causing systemic coagulopathy and inflammation following TBI remains unclear. In prior research, we discovered that brain-derived extracellular vesicles (BDEVs), originating from the injured brain, can activate the coagulation cascade and inflammatory cells. In this study, we primarily investigated how BDEVs affect systemic coagulopathy and inflammation in peripheral circulation. The results of cytokines and coagulation function indicated that BDEVs can lead to systemic coagulopathy and inflammation by influencing inflammatory factors and chemokines within 24 h. Furthermore, according to flow cytometry and blood cell counter results, we found that BDEVs induced changes in the blood count such as a reduced number of platelets and leukocytes and an increased percentage of neutrophils, macrophages, activated platelets, circulating platelet-EVs, and leukocyte-derived EVs. We also discovered that eliminating circulating BDEVs with lactadherin helped improve coagulopathy and inflammation, relieved blood cell dysfunction, and decreased the circulating platelet-EVs and leukocyte-derived EVs. Our research provides a novel viewpoint and potential mechanism of TBI-associated secondary damage.Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.

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出版当年[2023]版:
大类 | 2 区 医学
小类 | 2 区 免疫学 2 区 药学
最新[2023]版:
大类 | 2 区 医学
小类 | 2 区 免疫学 2 区 药学
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Q1 PHARMACOLOGY & PHARMACY Q2 IMMUNOLOGY
最新[2023]版:
Q1 PHARMACOLOGY & PHARMACY Q2 IMMUNOLOGY

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

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第一作者机构: [1]Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, China [2]Tianjin Neurological Institute, Tianjin, China [3]Graduate School, Tianjin Medical University, Tianjin, China [4]Key Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous System, Ministry of Education, Tianjin, China [5]Tianjin Key Laboratory of Injuries, Variations and Regeneration of Nervous System, Tianjin, China
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通讯机构: [1]Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, China [2]Tianjin Neurological Institute, Tianjin, China [4]Key Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous System, Ministry of Education, Tianjin, China [5]Tianjin Key Laboratory of Injuries, Variations and Regeneration of Nervous System, Tianjin, China [*1]Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, China
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