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Understanding risk of thrombosis with thrombocytopenia syndrome after Ad26.COV2.S vaccination

《医学前沿(英文)》 2021年 第15卷 第6期   页码 938-941 doi: 10.1007/s11684-021-0895-9

Epidemiology, pathogenesis, and management of coronavirus disease 2019-associated stroke

《医学前沿(英文)》 doi: 10.1007/s11684-023-1041-7

摘要: The coronavirus disease 2019 (COVID-19) epidemic has triggered a huge impact on healthcare, socioeconomics, and other aspects of the world over the past three years. An increasing number of studies have identified a complex relationship between COVID-19 and stroke, although active measures are being implemented to prevent disease transmission. Severe COVID-19 may be associated with an increased risk of stroke and increase the rates of disability and mortality, posing a serious challenge to acute stroke diagnosis, treatment, and care. This review aims to provide an update on the influence of COVID-19 itself or vaccines on stroke, including arterial stroke (ischemic stroke and hemorrhagic stroke) and venous stroke (cerebral venous thrombosis). Additionally, the neurovascular mechanisms involved in SARS-CoV-2 infection and the clinical characteristics of stroke in the COVID-19 setting are presented. Evidence on vaccinations, potential therapeutic approaches, and effective strategies for stroke management has been highlighted.

关键词: SARS-CoV-2     ischemic stroke     stroke     hemorrhagic stroke     cerebral venous thrombosis     vaccination    

Anti-β2GPI/β2GPI complexes induce platelet activation and promote thrombosis via

Wenjing Zhang, Caijun Zha, Xiumin Lu, Ruichun Jia, Fei Gao, Qi Sun, Meili Jin, Yanhong Liu

《医学前沿(英文)》 2019年 第13卷 第6期   页码 680-689 doi: 10.1007/s11684-018-0673-5

摘要: Anti- glycoprotein I (anti- GPI) antibodies are important contributors to the development of thrombosis. Anti- GPI antibody complexes with GPI are well known to activate monocytes and endothelial cells via the intracellular NF- B pathway with prothrombotic implications. By contrast, the interaction of anti- GPI/ GPI complexes with platelets has not been extensively studied. The p38 mitogen-activated protein kinase (MAPK) pathway has been recognized to be an important intracellular signaling pathway in the coagulation cascade and an integral component of arterial and venous thrombosis. The present study reveals that levels of anti- GPI/ GPI complexes in sera are positively associated with p38MAPK phosphorylation of platelets in thrombotic patients. Furthermore, SB203580 inhibits anti- GPI/ GPI complex-induced platelet activation. Thrombus formation decreased in mice after treatment with anti- GPI/ GPI complexes. In conclusion, p38MAPK may be a treatment target for anti- GPI antibody-associated thrombotic events.

关键词: anti-   

Endogenous tissue factor pathway inhibitor in vascular smooth muscle cells inhibits arterial thrombosis

null

《医学前沿(英文)》 2017年 第11卷 第3期   页码 403-409 doi: 10.1007/s11684-017-0522-y

摘要:

Tissue factor pathway inhibitor (TFPI) is the main inhibitor of tissue factor-mediated coagulation. TFPI is expressed by endothelial and smooth muscle cells in the vasculature. Endothelium-derived TFPI has been reported to play a regulatory role in arterial thrombosis. However, the role of endogenous TFPI in vascular smooth muscle cells (VSMCs) in thrombosis and vascular disease development has yet to be elucidated. In this TFPIFlox mice crossbred with Sma–Cre mice were utilized to establish TFPI conditional knockout mice and to examine the effects of VSMC-directed TFPI deletion on development, hemostasis, and thrombosis. The mice with deleted TFPI in VSMCs (TFPISma) reproduced viable offspring. Plasma TFPI concentration was reduced 7.2% in the TFPISma mice compared with TFPIFlox littermate controls. Plasma TFPI concentration was also detected in the TFPITie2 (mice deleted TFPI in endothelial cells and cells of hematopoietic origin) mice. Plasma TFPI concentration of the TFPITie2 mice was 80.4% lower (P<0.001) than that of the TFPIFlox mice. No difference in hemostatic measures (PT, APTT, and tail bleeding) was observed between TFPISma and TFPIFlox mice. However, TFPISma mice had increased ferric chloride–induced arterial thrombosis compared with TFPIFlox littermate controls. Taken together, these data indicated that endogenous TFPI from VSMCs inhibited ferric chloride–induced arterial thrombosis without causing hemostatic effects.

关键词: arterial thrombosis     conditional knockout mice     tissue factor pathway inhibitor     vascular smooth muscle cells    

Anti-β glycoprotein I antibodies in complex with β2 glycoprotein I induce platelet activation via two receptors: apolipoprotein E receptor 2' and glycoprotein I bα

null

《医学前沿(英文)》 2016年 第10卷 第1期   页码 76-84 doi: 10.1007/s11684-015-0426-7

摘要:

Anti-β2 glycoprotein I (anti-β2GP I ) antibodies are important contributors to thrombosis, especially in patients with antiphospholipid syndrome (APS). However, the mechanism by which anti-β2GP I antibodies are involved in the pathogenesis of thrombosis is not fully understood. In this report, we investigated the role of anti-β2GP I antibodies in complexes with β2GP I as mediators of platelet activation, which can serve as a potential source contributing to thrombosis. We examined the involvement of the apolipoprotein E receptor 2' (apoER2') and glycoprotein I ba (GP I bα) in platelet activation induced by the anti-β2GP I /β2GP I complex. The interaction between the anti-β2GP I /β2GP I complex and platelets was examined using in vitro methods, in which the Fc portion of the antibody was immobilized using protein A coated onto a microtiter plate. Platelet activation was assessed by measuring GP II b/ III a activation and P-selectin expression and thromboxane B2 production as well as p38 mitogen-activated protein kinase phosphorylation. Our results revealed that the anti-β2GP I /β2GP I complex was able to activate platelets, and this activation was inhibited by either the anti-GP I bα antibody or the apoER2' inhibitor. Results showed that the anti-β2GP I /β2GP I complex induced platelet activation via GP I bα and apoER2', which may then contribute to the prothrombotic tendency in APS patients.

关键词: anti-β2GP I /β2GP I complex     platelet     GP I bα     apoER2'     thrombosis    

标题 作者 时间 类型 操作

Understanding risk of thrombosis with thrombocytopenia syndrome after Ad26.COV2.S vaccination

期刊论文

Epidemiology, pathogenesis, and management of coronavirus disease 2019-associated stroke

期刊论文

Anti-β2GPI/β2GPI complexes induce platelet activation and promote thrombosis via

Wenjing Zhang, Caijun Zha, Xiumin Lu, Ruichun Jia, Fei Gao, Qi Sun, Meili Jin, Yanhong Liu

期刊论文

Endogenous tissue factor pathway inhibitor in vascular smooth muscle cells inhibits arterial thrombosis

null

期刊论文

Anti-β glycoprotein I antibodies in complex with β2 glycoprotein I induce platelet activation via two receptors: apolipoprotein E receptor 2' and glycoprotein I bα

null

期刊论文