ArticleCellular & molecular immunology2017
Arterial thrombosis in the context of HCV-associated vascular disease can be prevented by protein C.
Article in Cellular & molecular immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Thrombotic risk in hepatitis C: Interplay between hepatic dysfunction, viral-driven inflammation, and cardiovascular consequences.World journal of virology · 2025Review
- Inhibitors of Polyphosphate and Neutrophil Extracellular Traps.Seminars in thrombosis and hemostasis · 2024Review
- Potential Immunoregulatory Mechanism of Plant Saponins: A Review.Molecules (Basel, Switzerland) · 2023Review
- Monitoring circulating platelet activity to predict cancer-associated thrombosis.Cell reports methods · 2023Article
- Perivascular Mesenchymal Stem/Stromal Cells, an Immune Privileged Niche for Viruses?International journal of molecular sciences · 2022Review
- Platelet Innate Immune Receptors and TLRs: A Double-Edged Sword.International journal of molecular sciences · 2021Review
- Old drug, new Trick? The rationale for the treatment of COVID-19 with activated protein C.Medical hypotheses · 2021Article
- Thrombocytopenia in Virus Infections.Journal of clinical medicine · 2021Review
- Role of Platelets in Detection and Regulation of Infection.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Understanding Infection-Induced Thrombosis: Lessons Learned From Animal Models.Frontiers in immunology · 2019Review
- Double-stranded DNA induces a prothrombotic phenotype in the vascular endothelium.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) infection is a major problem worldwide. HCV is not limited to liver disease but is frequently complicated by immune-mediated extrahepatic manifestations such as glomerulonephritis or vasculitis. A fatal complication of HCV-associated vascular disease is thrombosis. Polyriboinosinic:polyribocytidylic acid (poly (I:C)), a synthetic analog of viral RNA, induces a Toll-like receptor 3 (TLR3)-dependent arteriolar thrombosis without significant thrombus formation in venules in vivo. These procoagulant effects are caused by increased endothelial synthesis of tissue factor and PAI-1 without platelet activation. In addition to human umbilical endothelial cells (HUVEC), human mesangial cells (HMC) produce procoagulatory factors, cytokines and adhesion molecules after stimulation with poly (I:C) or HCV-containing cryoprecipitates from a patient with a HCV infection as well. Activated protein C (APC) is able to prevent the induction of procoagulatory factors in HUVEC and HMC in vitro and blocks the effects of poly (I:C) and HCV-RNA on the expression of cytokines and adhesion molecules in HMC but not in HUVEC. In vivo, protein C inhibits poly (I:C)-induced arteriolar thrombosis. Thus, endothelial cells are de facto able to actively participate in immune-mediated vascular thrombosis caused by viral infections. Finally, we provide evidence for the ability of protein C to inhibit TLR3-mediated arteriolar thrombosis caused by HCV infection.
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Registered trials
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