| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Articles in PresS, published online ahead of print August 16, 2002
J Appl Physiol, 10.1152/jap.00451.2002
Submitted on May 20, 2002
Accepted on August 12, 2002
1 Physiological Sciences, University of Arizona, Tucson, AZ, USA
2 Department of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati, Cincinnati, OH, USA
3 Biomedical Engineering Programs, University of Arizona, Tucson, AZ, USA; Physiological Sciences, University of Arizona, Tucson, AZ, USA
* To whom correspondence should be addressed. E-mail: cjsulliv{at}u.arizona.edu.
Ischemic revascularization involves extensive structural adaptation of the vasculature, including both angiogenesis and arteriogenesis. Previous studies suggest that fibroblast growth factor-2 (FGF2) participates in both angiogenesis and arteriogenesis. Despite this, the specific role of endogenous FGF2 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 FGF2 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 post-surgery in both genotypes. Given the equivalent responses observed in Fgf2+/+ and Fgf2-/- mice, we demonstrate that endogenous FGF2 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 FGF2 in this model.
This article has been cited by other articles:
|
|
 |
|
  J.-W. Lin, W. H.-H. Sheu, W.-J. Lee, Y.-T. Chen, T.-J. Liu, C.-T. Ting, and W.-L. Lee Circulating Hepatocyte Growth Factor Level but Not Basic Fibroblast Growth Factor Level Is Elevated in Angiography-Proven Symptomatic Peripheral Artery Disease Angiology, September 1, 2007; 58(4): 420 - 428. [Abstract] [PDF]
|
|
|
|
 |
|
 F. Michel, J.-S. Silvestre, L. Waeckel, S. Corda, T. Verbeuren, J. P. Vilaine, M. Clergue, M. Duriez, and B. I. Levy Thromboxane A2/Prostaglandin H2 Receptor Activation Mediates Angiotensin II-Induced Postischemic Neovascularization Arterioscler Thromb Vasc Biol, March 1, 2006; 26(3): 488 - 493. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Gruionu, J. B. Hoying, L. G. Gruionu, M. H. Laughlin, and T. W. Secomb Structural adaptation increases predicted perfusion capacity after vessel obstruction in arteriolar arcade network of pig skeletal muscle Am J Physiol Heart Circ Physiol, June 1, 2005; 288(6): H2778 - H2784. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Gruionu, J. B. Hoying, A. R. Pries, and T. W. Secomb Structural remodeling of mouse gracilis artery after chronic alteration in blood supply Am J Physiol Heart Circ Physiol, May 1, 2005; 288(5): H2047 - H2054. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. L. Unthank, K. M. Sheridan, and M. C. Dalsing Collateral Growth in the Peripheral Circulation: A Review Vascular and Endovascular Surgery, July 1, 2004; 38(4): 291 - 313. [Abstract] [PDF]
|
|
|
|
 |
|
 S. L. House, C. Bolte, M. Zhou, T. Doetschman, R. Klevitsky, G. Newman, and J. E. J. Schultz Cardiac-Specific Overexpression of Fibroblast Growth Factor-2 Protects Against Myocardial Dysfunction and Infarction in a Murine Model of Low-Flow Ischemia Circulation, December 23, 2003; 108(25): 3140 - 3148. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
