NDLI: Induction of heme oxygenase-1 is a beneficial response in a murine model of venous thrombosis.

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Induction of heme oxygenase-1 is a beneficial response in a murine model of venous thrombosis.

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Induction of heme oxygenase-1 is a beneficial response in a murine model of venous thrombosis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Tracz, Michal J. Juncos, Julio P. Grande, Joseph P. Croatt, Anthony J. Ackerman, Allan W. Katusic, Zvonimir S. Nath, Karl A.
Description	Country affiliation: United States Author Affiliation: Tracz MJ ( Division of Nephrology and Hypertension, Department of Pathology, Mayo Clinic, Rochester, MN 55905, USA.)
Abstract	The induction of heme oxygenase-1 (HO-1) may protect against tissue injury. The present study examines the induction of HO-1 in a murine model of venous thrombosis and explores the downstream consequences of this induction. In a model of stasis-induced thrombosis created by ligation of the inferior vena cava, HO-1 expression is markedly induced. Such expression occurs primarily in smooth muscle cells in the venous wall and in leukocytes infiltrating the venous wall and clot. To determine the significance of HO-1 induction in venous thrombosis, this model was imposed in HO-1(+/+) and HO-1(-/-) mice. The initial clot size did not differ in either group by day 2, but was significantly larger in HO-1(-/-) mice by day 10, where an exaggerated inflammatory response in the venous wall was also observed. Following ligation of the inferior vena cava, HO-1(-/-) mice exhibited increased nuclear factor kappaB activation and markedly increased up-regulation of tissue factor, selectins, inflammatory cytokines, and matrix metalloproteinase-9, the latter incriminated in both clot lysis and vascular injury. We conclude that HO-1 deficiency impairs thrombus resolution and exaggerates the inflammatory response to thrombus formation. These findings offer insight into recent observations that polymorphisms in the HO-1 gene may increase the risk for recurrent venous thrombosis and dysfunction of hemodialysis arteriovenous fistulas, the latter caused, in part, by thrombosis.
File Format	HTM / HTML
ISSN	00029440
e-ISSN	15252191
DOI	10.2353/ajpath.2008.080556
Journal	The American Journal of Pathology
Issue Number	6
Volume Number	173
Language	English
Publisher	Elsevier (on behalf of the American Society for Investigative Pathology)
Publisher Date	2008-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Vena Cava, Inferior Research Support, N.i.h., Extramural Venous Thrombosis Interleukin-6 Chemokine Cxcl12 Surgery Heme Oxygenase-1 Genetics Disease Models, Animal Nf-kappa B Enzyme Induction Chemokine Cxcl1 Discipline Pathology Metabolism Thrombosis Mice, Knockout Thromboplastin Pathology Animals Mice Chemokine Ccl2 Matrix Metalloproteinase 9
Content Type	Text
Resource Type	Article
Subject	Pathology and Forensic Medicine

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Induction of Heme Oxygenase-1 is a Beneficial Response in a Murine Model of Venous Thrombosis

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