The thrombomodulin–protein C system is essential for the maintenance of pregnancy View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2003-03

AUTHORS

Berend Isermann, Rashmi Sood, Rafal Pawlinski, Mark Zogg, Shawn Kalloway, Jay L. Degen, Nigel Mackman, Hartmut Weiler

ABSTRACT

Disruption of the mouse gene encoding the blood coagulation inhibitor thrombomodulin (Thbd) leads to embryonic lethality caused by an unknown defect in the placenta. We show that the abortion of thrombomodulin-deficient embryos is caused by tissue factor-initiated activation of the blood coagulation cascade at the feto-maternal interface. Activated coagulation factors induce cell death and growth inhibition of placental trophoblast cells by two distinct mechanisms. The death of giant trophoblast cells is caused by conversion of the thrombin substrate fibrinogen to fibrin and subsequent formation of fibrin degradation products. In contrast, the growth arrest of trophoblast cells is not mediated by fibrin, but is a likely result of engagement of protease-activated receptors (PAR)-2 and PAR-4 by coagulation factors. These findings show a new function for the thrombomodulin-protein C system in controlling the growth and survival of trophoblast cells in the placenta. This function is essential for the maintenance of pregnancy. More... »

PAGES

331-337

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nm825

DOI

http://dx.doi.org/10.1038/nm825

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1027344353

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/12579195


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HOW TO GET THIS DATA PROGRAMMATICALLY:

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Turtle is a human-readable linked data format.

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RDF/XML is a standard XML format for linked data.

curl -H 'Accept: application/rdf+xml' 'https://scigraph.springernature.com/pub.10.1038/nm825'


 

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