Journal
SCIENCE
Volume 296, Issue 5574, Pages 1880-1882Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1071699
Keywords
-
Categories
Funding
- NHLBI NIH HHS [P01-HL16411] Funding Source: Medline
Ask authors/readers for more resources
The coagulant and inflammatory exacerbation in sepsis is counterbalanced by the protective protein C (PC) pathway. Activated PC (APC) was shown to use the endothelial cell PC receptor (EPCR) as a coreceptor for cleavage of protease activated receptor 1 (PAR1) on endothelial cells. Gene profiling demonstrated that PAR1 signaling could account for all APC-induced protective genes, including the immunomodulatory monocyte chemoattractant protein-1 (MCP-1), which was selectively induced by activation of PAR1, but not PAR2. Thus, the prototypical thrombin receptor is the target for EPCR-dependent APC signaling, suggesting a role for this receptor cascade in protection from sepsis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available