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1 Physiological Sciences and 3 Biomedical Engineering Programs, University of Arizona, Tucson, Arizona 85724; and 2 Department of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati, Cincinnati, Ohio 45221
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.
revascularization; angiogenesis; basic fibroblast growth factor; arteriogenesis; collateralization
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