| First Author | Sullivan CJ | Year | 2002 |
| Journal | J Appl Physiol (1985) | Volume | 93 |
| Issue | 6 | Pages | 2009-17 |
| PubMed ID | 12391121 | Mgi Jnum | J:103383 |
| Mgi Id | MGI:3609305 | Doi | 10.1152/japplphysiol.00451.2002 |
| Citation | Sullivan CJ, et al. (2002) Targeted disruption of the Fgf2 gene does not affect vascular growth in the mouse ischemic hindlimb. J Appl Physiol 93(6):2009-17 |
| abstractText | 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. |
