Targeted disruption of the Fgf2 gene does not affect vascular growth in the mouse ischemic hindlimb

Chris J. Sullivan, Thomas Doetschman, James B. Hoying

Research output: Contribution to journalArticle

39 Scopus citations

Abstract

Ischemic revascularization involves extensive structural adaptation of the vasculature, including both angiogenesis and arteriogenesis. Previous studies suggest that fibroblast growth factor (FGF)-2 participates in both angiogenesis and arteriogenesis. Despite this, the specific role of endogenous FGF-2 in vascular adaptation during ischemic revascularization is unknown. Therefore, we used femoral artery ligation in Fgf2+/+ and Fgf2-/- mice to test the hypothesis that endogenous FGF-2 is an important regulator of angiogenesis and arteriogenesis in the setting of hindlimb ischemia. Femoral ligation increased capillary and arteriole density in the ischemic calf in both Fgf2+/+ and Fgf2-/- mice. The level of angiographically visible arteries in the thigh was increased in the ischemic hindlimb in all mice, and no significant differences were observed between Fgf2+/+ and Fgf2-/- mice. Additionally, limb perfusion progressively improved to peak values at day 35 postsurgery in both genotypes. Given the equivalent responses observed in Fgf2+/+ and Fgf2-/- mice, we demonstrate that endogenous FGF-2 is not required for revascularization in the setting of peripheral ischemia. Vascular adaptation, including both angiogenesis and arteriogenesis, was not affected by the absence of FGF-2 in this model.

Original languageEnglish (US)
Pages (from-to)2009-2017
Number of pages9
JournalJournal of Applied Physiology
Volume93
Issue number6
DOIs
StatePublished - Dec 2002

Keywords

  • Angiogenesis
  • Arteriogenesis
  • Basic fibroblast growth factor
  • Collateralization
  • Revascularization

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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