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Title: Tissue factor deficiency causes cardiac fibrosis and left ventricular dysfunction
Authors: Pawlinski, R ×
Fernandes, A
Kehrle, B
Pedersen, B
Parry, G
Erlich, J
Pyo, R
Gutstein, D
Zhang, J
Castellino, F
Melis, Els
Carmeliet, Peter
Baretton, G
Luther, T
Taubman, M
Rosen, E
Mackman, N #
Issue Date: Nov-2002
Series Title: Proceedings of the National Academy of Sciences of the United States of America vol:99 issue:24 pages:15333-8
Abstract: Exposure of blood to tissue factor (TF) activates the extrinsic (TF:FVIIa) and intrinsic (FVIIIa:FIXa) pathways of coagulation. In this study, we found that mice expressing low levels of human TF ( approximately 1% of wild-type levels) in an mTF(-/-) background had significantly shorter lifespans than wild-type mice, in part, because of spontaneous fatal hemorrhages. All low-TF mice exhibited a selective heart defect that consisted of hemosiderin deposition and fibrosis. Direct intracardiac measurement demonstrated a 30% reduction (P < 0.001) in left ventricular function in 8-month-old low-TF mice compared with age-matched wild-type mice. Mice expressing low levels of murine FVII ( approximately 1% of wild-type levels) exhibited a similar pattern of hemosiderin deposition and fibrosis in their hearts. In contrast, FIX(-/-) mice, a model of hemophilia B, had normal hearts. Cardiac fibrosis in low-TF and low-FVII mice appears to be caused by hemorrhage from cardiac vessels due to impaired hemostasis. We propose that TF expression by cardiac myocytes provides a secondary hemostatic barrier to protect the heart from hemorrhage.
ISSN: 0027-8424
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Faculty of Medicine - miscellaneous
Molecular and Vascular Biology
Biomedical Sciences Teaching Methodology and Practicals
Laboratory of Angiogenesis and Vascular Metabolism (VIB-KU Leuven Centre for Cancer Biology) (+)
× corresponding author
# (joint) last author

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