Crucial role of the protein C pathway in governing microvascular inflammation in inflammatory bowel disease

Endothelial protein C receptor (EPCR) and thrombomodulin (TM) are expressed at high levels in the resting microvasculature and convert protein C (PC) into its activated form, which is a potent anticoagulant and antiinflammatory molecule. Here we provide evidence that in Crohn disease (CD) and ulcera...

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Veröffentlicht in:	The Journal of clinical investigation Jg. 117; H. 7; S. 1951 - 1960
Hauptverfasser:	Scaldaferri, Franco, Sans, Miquel, Vetrano, Stefania, Graziani, Cristina, De Cristofaro, Raimondo, Gerlitz, Bruce, Repici, Alessandro, Arena, Vincenzo, Malesci, Alberto, Panes, Julian, Grinnell, Brian W., Danese, Silvio
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States American Society for Clinical Investigation 01.07.2007
Schlagworte:	Animals Antigens, CD - metabolism Biomedical research Cell Adhesion - drug effects Cells, Cultured Chemokines - biosynthesis Colorectal diseases Down-Regulation Endothelial Protein C Receptor Endothelium - pathology Gastrointestinal diseases Humans Immunohistochemistry Inflammation Inflammation - metabolism Inflammation - pathology Inflammatory bowel disease Inflammatory Bowel Diseases - metabolism Inflammatory Bowel Diseases - pathology Intercellular Adhesion Molecule-1 - metabolism Leukocytes - cytology Mice Microcirculation - metabolism Microcirculation - pathology Protein C Protein C - metabolism Protein C - pharmacology Receptors, Cell Surface - metabolism Signal Transduction - drug effects Thrombomodulin - metabolism Tumor Necrosis Factor-alpha - pharmacology Vascular Cell Adhesion Molecule-1 - metabolism United States
ISSN:	0021-9738, 1558-8238
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Abstract	Endothelial protein C receptor (EPCR) and thrombomodulin (TM) are expressed at high levels in the resting microvasculature and convert protein C (PC) into its activated form, which is a potent anticoagulant and antiinflammatory molecule. Here we provide evidence that in Crohn disease (CD) and ulcerative colitis (UC), the 2 major forms of inflammatory bowel disease (IBD), there was loss of expression of endothelial EPCR and TM, which in turns caused impairment of PC activation by the inflamed mucosal microvasculature. In isolated human intestinal endothelial cells, administration of recombinant activated PC had a potent antiinflammatory effect, as demonstrated by downregulated cytokine-dependent cell adhesion molecule expression and chemokine production as well as inhibited leukocyte adhesion. In vivo, administration of activated PC was therapeutically effective in ameliorating experimental colitis as evidenced by reduced weight loss, disease activity index, and histological colitis scores as well as inhibited leukocyte adhesion to the inflamed intestinal vessels. The results suggest that the PC pathway represents a new system crucially involved in governing intestinal homeostasis mediated by the mucosal microvasculature. Restoring the PC pathway may represent a new therapeutic approach to suppress intestinal inflammation in IBD.
AbstractList	Endothelial protein C receptor (EPCR) and thrombomodulin (TM) are expressed at high levels in the resting microvasculature and convert protein C (PC) into its activated form, which is a potent anticoagulant and antiinflammatory molecule. Here we provide evidence that in Crohn disease (CD) and ulcerative colitis (UC), the 2 major forms of inflammatory bowel disease (IBD), there was loss of expression of endothelial EPCR and TM, which in turns caused impairment of PC activation by the inflamed mucosal microvasculature. In isolated human intestinal endothelial cells, administration of recombinant activated PC had a potent antiinflammatory effect, as demonstrated by downregulated cytokine-dependent cell adhesion molecule expression and chemokine production as well as inhibited leukocyte adhesion. In vivo, administration of activated PC was therapeutically effective in ameliorating experimental colitis as evidenced by reduced weight loss, disease activity index, and histological colitis scores as well as inhibited leukocyte adhesion to the inflamed intestinal vessels. The results suggest that the PC pathway represents a new system crucially involved in governing intestinal homeostasis mediated by the mucosal microvasculature. Restoring the PC pathway may represent a new therapeutic approach to suppress intestinal inflammation in IBD. Endothelial protein C receptor (EPCR) and thrombomodulin (TM) are expressed at high levels in the resting microvasculature and convert protein C (PC) into its activated form, which is a potent anticoagulant and antiinflammatory molecule. Here we provide evidence that in Crohn disease (CD) and ulcerative colitis (UC), the 2 major forms of inflammatory bowel disease (IBD), there was loss of expression of endothelial EPCR and TM, which in turns caused impairment of PC activation by the inflamed mucosal microvasculature. In isolated human intestinal endothelial cells, administration of recombinant activated PC had a potent antiinflammatory effect, as demonstrated by downregulated cytokine-dependent cell adhesion molecule expression and chemokine production as well as inhibited leukocyte adhesion. In vivo, administration of activated PC was therapeutically effective in ameliorating experimental colitis as evidenced by reduced weight loss, disease activity index, and histological colitis scores as well as inhibited leukocyte adhesion to the inflamed intestinal vessels. The results suggest that the PC pathway represents a new system crucially involved in governing intestinal homeostasis mediated by the mucosal microvasculature. Restoring the PC pathway may represent a new therapeutic approach to suppress intestinal inflammation in IBD.Endothelial protein C receptor (EPCR) and thrombomodulin (TM) are expressed at high levels in the resting microvasculature and convert protein C (PC) into its activated form, which is a potent anticoagulant and antiinflammatory molecule. Here we provide evidence that in Crohn disease (CD) and ulcerative colitis (UC), the 2 major forms of inflammatory bowel disease (IBD), there was loss of expression of endothelial EPCR and TM, which in turns caused impairment of PC activation by the inflamed mucosal microvasculature. In isolated human intestinal endothelial cells, administration of recombinant activated PC had a potent antiinflammatory effect, as demonstrated by downregulated cytokine-dependent cell adhesion molecule expression and chemokine production as well as inhibited leukocyte adhesion. In vivo, administration of activated PC was therapeutically effective in ameliorating experimental colitis as evidenced by reduced weight loss, disease activity index, and histological colitis scores as well as inhibited leukocyte adhesion to the inflamed intestinal vessels. The results suggest that the PC pathway represents a new system crucially involved in governing intestinal homeostasis mediated by the mucosal microvasculature. Restoring the PC pathway may represent a new therapeutic approach to suppress intestinal inflammation in IBD.
Audience	Academic
Author	De Cristofaro, Raimondo Arena, Vincenzo Scaldaferri, Franco Danese, Silvio Graziani, Cristina Grinnell, Brian W. Sans, Miquel Vetrano, Stefania Panes, Julian Gerlitz, Bruce Malesci, Alberto Repici, Alessandro
AuthorAffiliation	1 Division of Gastroenterology, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Istituto Clinico Humanitas, Rozzano, Italy. 2 Institute of Internal Medicine, Catholic University, Rome, Italy. 3 Department of Gastroenterology, Hospital Clinic y Provincial, Barcelona, Spain. 4 Biotechnology Discovery Research, Lilly Research Laboratories, Indianapolis, Indiana, USA. 5 Department of Pathology, Catholic University, Rome, Italy
AuthorAffiliation_xml	– name: 1 Division of Gastroenterology, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Istituto Clinico Humanitas, Rozzano, Italy. 2 Institute of Internal Medicine, Catholic University, Rome, Italy. 3 Department of Gastroenterology, Hospital Clinic y Provincial, Barcelona, Spain. 4 Biotechnology Discovery Research, Lilly Research Laboratories, Indianapolis, Indiana, USA. 5 Department of Pathology, Catholic University, Rome, Italy
Author_xml	– sequence: 1 givenname: Franco surname: Scaldaferri fullname: Scaldaferri, Franco – sequence: 2 givenname: Miquel surname: Sans fullname: Sans, Miquel – sequence: 3 givenname: Stefania surname: Vetrano fullname: Vetrano, Stefania – sequence: 4 givenname: Cristina surname: Graziani fullname: Graziani, Cristina – sequence: 5 givenname: Raimondo surname: De Cristofaro fullname: De Cristofaro, Raimondo – sequence: 6 givenname: Bruce surname: Gerlitz fullname: Gerlitz, Bruce – sequence: 7 givenname: Alessandro surname: Repici fullname: Repici, Alessandro – sequence: 8 givenname: Vincenzo surname: Arena fullname: Arena, Vincenzo – sequence: 9 givenname: Alberto surname: Malesci fullname: Malesci, Alberto – sequence: 10 givenname: Julian surname: Panes fullname: Panes, Julian – sequence: 11 givenname: Brian W. surname: Grinnell fullname: Grinnell, Brian W. – sequence: 12 givenname: Silvio surname: Danese fullname: Danese, Silvio
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/17557119$$D View this record in MEDLINE/PubMed
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Snippet	Endothelial protein C receptor (EPCR) and thrombomodulin (TM) are expressed at high levels in the resting microvasculature and convert protein C (PC) into its...
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SubjectTerms	Animals Antigens, CD - metabolism Biomedical research Cell Adhesion - drug effects Cells, Cultured Chemokines - biosynthesis Colorectal diseases Down-Regulation Endothelial Protein C Receptor Endothelium - pathology Gastrointestinal diseases Humans Immunohistochemistry Inflammation Inflammation - metabolism Inflammation - pathology Inflammatory bowel disease Inflammatory Bowel Diseases - metabolism Inflammatory Bowel Diseases - pathology Intercellular Adhesion Molecule-1 - metabolism Leukocytes - cytology Mice Microcirculation - metabolism Microcirculation - pathology Protein C Protein C - metabolism Protein C - pharmacology Receptors, Cell Surface - metabolism Signal Transduction - drug effects Thrombomodulin - metabolism Tumor Necrosis Factor-alpha - pharmacology Vascular Cell Adhesion Molecule-1 - metabolism
Title	Crucial role of the protein C pathway in governing microvascular inflammation in inflammatory bowel disease
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