Heme Oxygenase-1/Carbon Monoxide Enhances Re-endothelialization in Vascular Injury

Strategic Insights -

Scientists in Taipei, Taiwan, have discovered that heme oxygenase-1 (HO-1), an enzyme with multiple vasoprotective functions, plays a crucial role in promoting the mobilization of circulating endothelial progenitor cells (EPCs) and enhancing re-endothelialization after vascular injury. The study, published in the Journal of Thrombosis and Haemostasis, found that systemic HO-1 expression led to elevated serum levels of vascular endothelial growth factor (VEGF) and stromal cell-derived factor-1 (SDF-1), resulting in an increase in circulating EPCs. The re-endothelialization of denuded vessels was accelerated in mice with systemic HO-1 overexpression, and the effect of carbon monoxide (CO), a byproduct of heme degradation by HO-1, was also assessed.

Key Takeaways:

  • Systemic HO-1 induction led to elevated serum levels of VEGF and SDF-1, resulting in an increase in circulating EPCs.
  • The re-endothelialization of denuded vessels was accelerated in mice with systemic HO-1 overexpression.
  • Carbon monoxide (CO) exposure prior to carotid injury also led to an increase in EPC mobilization and re-endothelialization.
  • The increase in EPC mobilization and enhanced re-endothelialization was associated with an increase in circulating SDF-1 but not VEGF.
  • Both EPC mobilization and re-endothelialization were significantly attenuated in mice with HO-1 deficiency.
  • The findings support a vital role of HO-1 and its reaction byproduct, CO, in vascular repair through enhancing EPC mobilization.

Statistics:

  • 250 p.p.m. CO was used for 2 h day(-1) to expose mice to CO.
  • 1401-8: The study was published in the Journal of Thrombosis and Haemostasis (2009;7(8):1401-8).

Sources:

  • Lin, H. H., et al. (2009). After vascular injury, heme oxygenase-1/carbon monoxide enhances re-endothelialization via promoting mobilization of circulating endothelial progenitor cells. Journal of Thrombosis and Haemostasis, 2009;7(8):1401-8.
  • National Yang-Ming University, Institute of Pharmacology.