Promotion of airway anastomotic microvascular regeneration and alleviation of airway ischemia by deferoxamine nanoparticles

Biomaterials. 2014 Jan;35(2):803-813. doi: 10.1016/j.biomaterials.2013.09.092. Epub 2013 Oct 22.

Abstract

Airway tissue ischemia and hypoxia in human lung transplantation is a consequence of the sacrifice of the bronchial circulation during the surgical procedure and is a major risk factor for the development of airway anastomotic complications. Augmented expression of hypoxia-inducible factor (HIF)-1α promotes microvascular repair and alleviates allograft ischemia and hypoxia. Deferoxamine mesylate (DFO) is an FDA-approved iron chelator which has been shown to upregulate cellular HIF-1α. Here, we developed a nanoparticle formulation of DFO that can be topically applied to airway transplants at the time of surgery. In a mouse orthotopic tracheal transplant (OTT) model, the DFO nanoparticle was highly effective in enhancing airway microvascular perfusion following transplantation through the production of the angiogenic factors, placental growth factor (PLGF) and stromal cell-derived factor (SDF)-1. The endothelial cells in DFO treated airways displayed higher levels of p-eNOS and Ki67, less apoptosis, and decreased production of perivascular reactive oxygen species (ROS) compared to vehicle-treated airways. In summary, a DFO formulation topically-applied at the time of surgery successfully augmented airway anastomotic microvascular regeneration and the repair of alloimmune-injured microvasculature. This approach may be an effective topical transplant-conditioning therapy for preventing airway complications following clinical lung transplantation.

Keywords: Bioabsorption; Nanoparticle; Oxygenation; Surface treatment; Transplantation; Wound healing.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Angiogenesis Inducing Agents / metabolism
  • Animals
  • Apoptosis / drug effects
  • Chemokine CXCL12 / genetics
  • Chemokine CXCL12 / metabolism
  • Deferoxamine / chemistry
  • Deferoxamine / pharmacology*
  • Endothelial Cells / metabolism
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit / genetics
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Ischemia / drug therapy*
  • Lung Transplantation / adverse effects
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Microvessels / drug effects*
  • Nanoparticles / chemistry*
  • Nitric Oxide Synthase Type III / genetics
  • Nitric Oxide Synthase Type III / metabolism
  • Placenta Growth Factor
  • Pregnancy Proteins / genetics
  • Pregnancy Proteins / metabolism
  • Promoter Regions, Genetic
  • Reactive Oxygen Species / metabolism
  • Regeneration / drug effects*
  • Swine
  • Trachea / drug effects
  • Trachea / transplantation

Substances

  • Angiogenesis Inducing Agents
  • Chemokine CXCL12
  • Cxcl12 protein, mouse
  • Hif1a protein, mouse
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • PGF protein, human
  • Pgf protein, mouse
  • Pregnancy Proteins
  • Reactive Oxygen Species
  • Placenta Growth Factor
  • Nitric Oxide Synthase Type III
  • Nos3 protein, mouse
  • Deferoxamine