Femoral artery neointimal hyperplasia is reduced after wire injury in Ref-1+/- mice

David L. Basi, Neeta Adhikari, Ami Mariash, Qinglu Li, Esther Kao, Sureni V. Mullegama, Jennifer L. Hall

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


Redox factor-1 (Ref-1) is a multifunctional protein that regulates redox, DNA repair, and the response to cell stress. We previously demonstrated that Ref-1+/- mice exhibit a significantly reduced Ref-1 mRNA and protein levels within the vasculature, which are associated with increased oxidative stress. The goal of this study was to test the hypothesis that partial loss of Ref-1 altered the cellular response to vascular injury. Fourteen days after femoral artery wire injury, we found that vessel intima-to-media ratio was significantly reduced in Ref-1+/- mice compared with that in wild-type mice (P < 0.01). Bromodeoxyuridine labeling and transferase-mediated dUTP nickend labeling staining at 14 days did not differ in the Ref-1+/- mice. In vitro studies found no significant changes in either serum-induced proliferation or baseline apoptosis in Ref-1+/- vascular smooth muscle cells. Exposure to Fas ligand; however, did result in increased susceptibility of Ref-1+/- vascular smooth muscle cells to apoptosis (P < 0.001). Ref-1+/- mice exhibited an increase in circulating baseline levels of IL-10, IL-1α, and VEGF compared with those in wild-type mice but a marked impairment in these pathways in response to injury. In sum, loss of a single allele of Ref-1 is sufficient to reduce intimal lesion formation and to alter circulating cytokine and growth factor expression.

Original languageEnglish (US)
Pages (from-to)H516-H521
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number1
StatePublished - Jan 1 2007


  • Inflammation
  • Neointima formation
  • Redox factor-1
  • Vascular biology
  • Vascular injury


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