The role of tissue factor pathway inhibitor in atherosclerosis and arterial thrombosis

Winckers, Kristien; Cate, Hugo Ten; Hackeng, Tilman M.

doi:10.1016/j.blre.2013.03.001

Cited by 83 publications

(66 citation statements)

References 148 publications

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“…While macrophages can turn into large foam cells after migrating to the subendothelial intima and internalizing oxLDL, they also produce cytokines, such as tumor necrosis factor-α (TNF-α), and chemokines, such as monocyte chemotactic protein-1 (MCP-1) 34) . As shown in recent studies, both cytokines and che- activation of the TLR4 downstream signaling molecule NF-κB was not completely inhibited by TLR4 gene mutation.…”

Section: Discussionmentioning

confidence: 99%

Involvement of TLR4 in Oxidized LDL/β2GPI/Anti-β2GPI-Induced Transformation of Macrophages to Foam Cells

Zhang

Xie

Zhou

et al. 2014

JAT

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Aim: It has been reported that oxidized low-density lipoprotein (oxLDL) forms a stable and non-dissociable complex with β2-glycoprotein I (β2GPI) and that IgG anti-β2GPI autoantibodies are able to recognize this complex, thus facilitating macrophage-derived foam cell formation in patients with antiphospholipid syndrome (APS). However, the immunopathological mechanisms of oxLDL/β2GPI complexes in promoting foam cell formation are not fully understood. In this study, we examined the role of toll-like receptor 4 (TLR4) in the oxLDL/β2GPI/anti-β2GPI complex-induced transformation of mouse peritoneal macrophages to foam cells.

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Section: Discussionmentioning

confidence: 99%

Involvement of TLR4 in Oxidized LDL/β2GPI/Anti-β2GPI-Induced Transformation of Macrophages to Foam Cells

Zhang

Xie

Zhou

et al. 2014

JAT

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“…In procoagulating conditions, like atherosclerotic plaques, TFPI colocalizes with TF, indicating an active role of TFPI in attenuating TF activity. 28 Alan Mast 29 recently reviewed the anticoagulation activities of TFPI and its clinical relevance. TFPI may be a promising target for treating thrombosis/bleeding disorders.…”

Section: Tissue Factormentioning

confidence: 99%

“…TFPI may be a promising target for treating thrombosis/bleeding disorders. [28][29][30] TFPI is believed to be secreted primarily by ECs, 27,31 thus could be an important messenger of ECs in modulating TF activities and thrombosis.…”

Section: Tissue Factormentioning

confidence: 99%

Thrombotic Regulation From the Endothelial Cell Perspectives

Wang

Hao

Leeper

et al. 2018

ATVB

117

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“…These results indicated that TFPI, DAG1 and CFLAR may play critical roles in EBOV GP-induced cell cytotoxicity. TFPI, DAG1 and CFLAR have been previously shown to be associated with cell adhesion [4043], while TFPI also plays a part in the inhibition of coagulation [44] and CFLAR has an inhibitory role in apoptosis [45]. Therefore, we sought to evaluate whether the rescue effect of cell viability could be enhanced when cells were treated with these proteins in combination.…”

Section: Forced Expression Of Tfpi Dag1 and Cflar Ameliorated Ebov Gmentioning

confidence: 99%

Hsa-miR-1246, hsa-miR-320a and hsa-miR-196b-5p inhibitors can reduce the cytotoxicity of Ebola virus glycoprotein in vitro

Sheng

Zhang

Chen

et al. 2014

Sci. China Life Sci.

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Ebola virus (EBOV) causes a highly lethal hemorrhagic fever syndrome in humans and has been associated with mortality rates of up to 91% in Zaire, the most lethal strain. Though the viral envelope glycoprotein (GP) mediates widespread inflammation and cellular damage, these changes have mainly focused on alterations at the protein level, the role of microRNAs (miRNAs) in the molecular pathogenesis underlying this lethal disease is not fully understood. Here, we report that the miRNAs hsa-miR-1246, hsa-miR-320a and hsa-miR-196b-5p were induced in human umbilical vein endothelial cells (HUVECs) following expression of EBOV GP. Among the proteins encoded by predicted targets of these miRNAs, the adhesion-related molecules tissue factor pathway inhibitor (TFPI), dystroglycan1 (DAG1) and the caspase 8 and FADD-like apoptosis regulator (CFLAR) were significantly downregulated in EBOV GP-expressing HUVECs. Moreover, inhibition of hsa-miR-1246, hsa-miR-320a and hsa-miR-196b-5p, or overexpression of TFPI, DAG1 and CFLAR rescued the cell viability that was induced by EBOV GP. Our results provide a novel molecular basis for EBOV pathogenesis and may contribute to the development of strategies to protect against future EBOV pandemics. Ebola virus, glycoprotein, microRNAs, cytotoxicity Citation:Sheng MM, Zhong Y, Chen Y, Du JC, Ju XW, Zhao C, Zhang GG, Zhang LF, Liu KT, Yang N, Xie P, Li DS, Zhang MQ, Jiang CY. Hsa-miR-1246, hsa-miR-320a and hsa-miR-196b-5p inhibitors can reduce the cytotoxicity of Ebola virus glycoprotein in vitro. Sci China Life Sci, 2014, 57: 959 -972,

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The role of tissue factor pathway inhibitor in atherosclerosis and arterial thrombosis

Cited by 83 publications

References 148 publications

Involvement of TLR4 in Oxidized LDL/β2GPI/Anti-β2GPI-Induced Transformation of Macrophages to Foam Cells

Involvement of TLR4 in Oxidized LDL/β2GPI/Anti-β2GPI-Induced Transformation of Macrophages to Foam Cells

Thrombotic Regulation From the Endothelial Cell Perspectives

Hsa-miR-1246, hsa-miR-320a and hsa-miR-196b-5p inhibitors can reduce the cytotoxicity of Ebola virus glycoprotein in vitro

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