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Organ-Specific Protection Against Lipopolysaccharide-Induced Vascular Leak Is Dependent on the Endothelial Protein C Receptor

Organ-Specific Protection Against Lipopolysaccharide-Induced Vascular Leak Is Dependent on the... Organ-Specific Protection Against Lipopolysaccharide- Induced Vascular Leak Is Dependent on the Endothelial Protein C Receptor Annette von Drygalski, Christian Furlan-Freguia, Wolfram Ruf, John H. Griffin, Laurent O. Mosnier Objective—To study the role of the endothelial protein C receptor (EPCR) in the modulation of susceptibility to inflammation- induced vascular leak in vivo. low Approach and Results—Genetically modified mice with low, <10% EPCR expression (EPCR ) 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- low wise analysis of EPCR 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 low in EPCR versus control mice in response to lipopolysaccharides. Histology of kidney and lung confirmed the EPCR- low specific pathology. In addition to severe kidney injury in response to lipopolysaccharides, EPCR and anti-EPCR– treated wild-type mice suffered from enhanced albuminuria and profound renal hemorrhage versus controls. Intravascular low volume loss at the same extent of weight loss in EPCR mice compared with control mice provided proof http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis, Thrombosis, and Vascular Biology Wolters Kluwer Health

Organ-Specific Protection Against Lipopolysaccharide-Induced Vascular Leak Is Dependent on the Endothelial Protein C Receptor

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References (45)

Copyright
© 2013 American Heart Association, Inc.
ISSN
1079-5642
eISSN
1524-4636
DOI
10.1161/ATVBAHA.112.301082
pmid
23393392
Publisher site
See Article on Publisher Site

Abstract

Organ-Specific Protection Against Lipopolysaccharide- Induced Vascular Leak Is Dependent on the Endothelial Protein C Receptor Annette von Drygalski, Christian Furlan-Freguia, Wolfram Ruf, John H. Griffin, Laurent O. Mosnier Objective—To study the role of the endothelial protein C receptor (EPCR) in the modulation of susceptibility to inflammation- induced vascular leak in vivo. low Approach and Results—Genetically modified mice with low, <10% EPCR expression (EPCR ) 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- low wise analysis of EPCR 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 low in EPCR versus control mice in response to lipopolysaccharides. Histology of kidney and lung confirmed the EPCR- low specific pathology. In addition to severe kidney injury in response to lipopolysaccharides, EPCR and anti-EPCR– treated wild-type mice suffered from enhanced albuminuria and profound renal hemorrhage versus controls. Intravascular low volume loss at the same extent of weight loss in EPCR mice compared with control mice provided proof

Journal

Arteriosclerosis, Thrombosis, and Vascular BiologyWolters Kluwer Health

Published: Apr 1, 2013

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