ArticleArteriosclerosis, thrombosis, and vascular biology2013
Organ-specific protection against lipopolysaccharide-induced vascular leak is dependent on the endothelial protein C receptor.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Protein C system defects inflicted by the malaria parasite protein PfEMP1 can be overcome by a soluble EPCR variant.Thrombosis and haemostasis · 2015Trial
- Sex differences in cardiovascular response to sepsis.American journal of physiology. Cell physiology · 2023Review
- Renal microvascular endothelial cell responses in sepsis-induced acute kidney injury.Nature reviews. Nephrology · 2022Review
- Unlocking the Untapped Potential of Endothelial Kinase and Phosphatase Involvement in Sepsis for Drug Treatment Design.Frontiers in immunology · 2022Review
- Pleiotropic actions of factor Xa inhibition in cardiovascular prevention: mechanistic insights and implications for anti-thrombotic treatment.Cardiovascular research · 2021Review
- Feeding-induced resistance to acute lethal sepsis is dependent on hepatic BMAL1 and FXR signalling.Nature communications · 2021Article
- TRPM7 mediates kidney injury, endothelial hyperpermeability and mortality during endotoxemia.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- The in vivo endothelial cell translatome is highly heterogeneous across vascular beds.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Mechanisms of vascular permeability and remodeling associated with hemarthrosis in factor VIII-deficient mice.Journal of thrombosis and haemostasis : JTH · 2019Article
- TAFI deficiency causes maladaptive vascular remodeling after hemophilic joint bleeding.JCI insight · 2019Article
- Activated protein C in neuroprotection and malaria.Current opinion in hematology · 2019Review
- Defective TAFI activation in hemophilia A mice is a major contributor to joint bleeding.Blood · 2018Article
- Vascular Permeability and Remodelling Coincide with Inflammatory and Reparative Processes after Joint Bleeding in Factor VIII-Deficient Mice.Thrombosis and haemostasis · 2018Article
- An ADAM-10 dependent EPCR shedding links meningococcal interaction with endothelial cells to purpura fulminans.PLoS pathogens · 2018Article
- Role of MiR-126a-3p in Endothelial Injury in Endotoxic Mice.Critical care medicine · 2016Article
- Heterozygous congenital Factor VII deficiency with the 9729del4 mutation, associated with severe spontaneous intracranial bleeding in an adolescent male.Blood cells, molecules & diseases · 2016Article
- The emerging role of coagulation proteases in kidney disease.Nature reviews. Nephrology · 2016Review
- Cell painting with an engineered EPCR to augment the protein C system.Thrombosis and haemostasis · 2015Article
- Vascular remodeling underlies rebleeding in hemophilic arthropathy.American journal of hematology · 2015Article
- Pro-Coagulant Endothelial Dysfunction Results from EHEC Shiga Toxins and Host Damage-Associated Molecular Patterns.Frontiers in immunology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo study the role of the endothelial protein C receptor (EPCR) in the modulation of susceptibility to inflammation-induced vascular leak in vivo. APPROACH AND
resultsGenetically modified mice with low, <10% EPCR expression (EPCR(low)) and control mice were challenged with lipopolysaccharides in a mouse model of endotoxemia. Infrared fluorescence and quantification of albumin-bound Evans Blue in tissues and intravascular plasma volumes were used to assess plasma extravasation. Pair-wise analysis of EPCR(low) and control mice matched for sex, age, and weight allowed determination of EPCR-dependent vascular leak. Kidney, lung, and brain were the organs with highest discriminative increased Evans Blue accumulation in EPCR(low) versus control mice in response to lipopolysaccharides. Histology of kidney and lung confirmed the EPCR-specific pathology. In addition to severe kidney injury in response to lipopolysaccharides, EPCR(low) and anti-EPCR-treated wild-type mice suffered from enhanced albuminuria and profound renal hemorrhage versus controls. Intravascular volume loss at the same extent of weight loss in EPCR(low) mice compared with control mice provided proof that plasma leak was the predominant cause of Evans Blue tissue accumulation.
conclusionsThis study demonstrates an important protective role for EPCR in vivo against vascular leakage during inflammation and suggests that EPCR-dependent vascular protection is organ-specific.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.