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- Title
Genetic deficiency of heme oxygenase-1 impairs functionality and form of an arteriovenous fistula in the mouse.
- Authors
Juncos, J. P.; Tracz, M. J.; Croatt, A. J.; Grande, J. P.; Ackerman, A. W.; Katusic, Z. S.; Nath, K. A.
- Abstract
Vascular access dysfunction contributes to patient morbidity during maintenance hemodialysis. In this study we determined if knockout of heme oxygenase-1 predisposed to malfunction of arteriovenous fistulas. After three weeks, all fistulas in wild type mice were patent whereas a third of the fistulas in knockout mice were occluded and these exhibited increased neointimal hyperplasia and venous wall thickening. Heme oxygenase-1 mRNA and protein were robustly induced in the fistulas of the wild type mice. In the knockout mice there was increased PAI-1 and MCP-1 expression, marked induction of MMP-2 and MMP-9, but similar expression of PDGFα, IGF-1, TGF-β1, VEGF, and osteopontin compared to wild type mice. We conclude that heme oxygenase-1 deficiency promotes vasculopathic gene expression, accelerates neointimal hyperplasia and impairs the function of arteriovenous fistulas.Kidney International (2008) 74, 47–51; doi:10.1038/ki.2008.110; published online 26 March 2008
- Subjects
GENETICS; EMBRYOLOGY; GENETIC disorders; GENE expression; MESSENGER RNA; CELL adhesion molecules; BIOMOLECULES
- Publication
Kidney International, 2008, Vol 74, Issue 1, p47
- ISSN
0085-2538
- Publication type
Article
- DOI
10.1038/ki.2008.110