Journal
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
Volume 28, Issue 9, Pages 1614-1620Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/ATVBAHA.107.158725
Keywords
VEGF-B; angiogenesis; arteriogenesis; collateral growth; cardiac ischemia; limb ischemia
Categories
Funding
- FWO [G0125.00, G.0121.02]
- EU [QLRT-200101955]
- Leducq foundation
- Concerted Research Activities [GOA2001/09, IAP-P5/02, IAP-P6/30]
- NIH [HL65572]
- Swedish Research Council
- Novo Nordisk Foundation
- Wallenbergs Foundation
- Karolinska Institute [DE 740/1-1]
Ask authors/readers for more resources
Objective-The endogenous role of the VEGF family member vascular endothelial growth factor-B (VEGF-B) in pathological angiogenesis remains unclear. Methods and Results-We studied the role of VEGF-B in various models of pathological angiogenesis using mice lacking VEGF-B (VEGF-B-/-) or overexpressing VEGF-B-167. After occlusion of the left coronary artery, VEGF-B deficiency impaired vessel growth in the ischemic myocardium whereas, in wild-type mice, VEGF-B-167 overexpression enhanced revascularization of the infarct and ischemic border zone. By contrast, VEGF-B deficiency did not affect vessel growth in the wounded skin, hypoxic lung, ischemic retina, or ischemic limb. Moreover, VEGF-B-167 overexpression failed to enhance vascular growth in the skin or ischemic limb. Conclusion-VEGF-B appears to have a relatively restricted angiogenic activity in the ischemic heart. These insights might offer novel therapeutic opportunities.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available