Format

Send to

Choose Destination
Kidney Int. 2008 Jul;74(1):47-51. doi: 10.1038/ki.2008.110. Epub 2008 Mar 26.

Genetic deficiency of heme oxygenase-1 impairs functionality and form of an arteriovenous fistula in the mouse.

Author information

1
Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota 55905, USA.

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 PDGF alpha, IGF-1, TGF-beta1, 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.

PMID:
18368029
PMCID:
PMC2914571
DOI:
10.1038/ki.2008.110
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center