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

J. P. Juncos, M. J. Tracz, A. J. Croatt, J. P. Grande, A. W. Ackerman, Z. S. Katusic, K. A. Nath

Research output: Contribution to journalArticlepeer-review

51 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)47-51
Number of pages5
JournalKidney international
Volume74
Issue number1
DOIs
StatePublished - Jul 2008

Keywords

  • Arteriovenous access
  • Arteriovenous fistula
  • Arteriovenous graft
  • Chronic dialysis
  • Heme oxygenase

ASJC Scopus subject areas

  • Nephrology

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