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pmid: 15477409
Background— Therapeutic angiogenesis by delivery of vascular endothelial growth factor (VEGF) has attracted attention. However, the role and function of VEGF in experimental restenosis (neointimal formation) after vascular intraluminal injury have not been addressed. Methods and Results— We report herein that blockade of VEGF by soluble VEGF receptor 1 ( sFlt-1 ) gene transfer attenuated neointimal formation after intraluminal injury in rabbits, rats, and mice. sFlt-1 gene transfer markedly attenuated the early vascular inflammation and proliferation and later neointimal formation. sFlt-1 gene transfer also inhibited increased expression of inflammatory factors such as monocyte chemoattractant protein-1 and VEGF. Intravascular VEGF gene transfer enhanced angiogenesis in the adventitia but did not reduce neointimal formation. Conclusions— Increased expression and activity of VEGF are essential in the development of experimental restenosis after intraluminal injury by recruiting monocyte-lineage cells.
Inflammation, Male, Extracellular Matrix Proteins, Hyperplasia, Genetic Vectors, Mice, Transgenic, Constriction, Pathologic, Genetic Therapy, Monocytes, Adenoviridae, Catheterization, Femoral Artery, Mice, Gene Expression Regulation, Animals, Cell Lineage, Endothelium, Vascular, Carotid Artery Injuries, Cell Division, Bone Marrow Transplantation
Inflammation, Male, Extracellular Matrix Proteins, Hyperplasia, Genetic Vectors, Mice, Transgenic, Constriction, Pathologic, Genetic Therapy, Monocytes, Adenoviridae, Catheterization, Femoral Artery, Mice, Gene Expression Regulation, Animals, Cell Lineage, Endothelium, Vascular, Carotid Artery Injuries, Cell Division, Bone Marrow Transplantation
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 127 | |
popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Top 10% | |
influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 1% |