Arterial thrombosis in the context of HCV-associated vascular disease can be prevented by protein C View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-12

AUTHORS

Philipp Blüm, Joachim Pircher, Monika Merkle, Thomas Czermak, Andrea Ribeiro, Hanna Mannell, Florian Krötz, Alexander Hennrich, Michael Spannagl, Simone Köppel, Erik Gaitzsch, Markus Wörnle

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. More... »

PAGES

986

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/cmi.2016.10

DOI

http://dx.doi.org/10.1038/cmi.2016.10

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1028276384

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27086952


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