Circulation · 2004
Blockade of vascular endothelial growth factor suppresses experimental restenosis after intraluminal injury by inhibiting recruitment of monocyte lineage cells.
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Ohtani Kisho, Egashira Kensuke, Hiasa Ken-ichi, Zhao Qingwei, Kitamoto Shiro, Ishibashi Minako, Usui Makoto, Inoue Shujiro, Yonemitsu Yoshikazu, Sueishi Katsuo, Sata Masataka, Shibuya Masabumi, Sunagawa Kenji
Аннотация
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.
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.
Предметные рубрики MeSH
AdenoviridaeAnimalsBone Marrow TransplantationCarotid Artery InjuriesCatheterizationCell DivisionCell LineageConstriction, PathologicEndothelium, VascularExtracellular Matrix ProteinsFemoral ArteryGene Expression RegulationGenetic TherapyGenetic VectorsHyperplasiaInflammationMaleMiceMice, TransgenicMonocytesMyosin Heavy ChainsNeovascularization, PhysiologicNonmuscle Myosin Type IIBProteinsRabbitsRatsRats, Inbred WKYReceptors, Vascular Endothelial Growth FactorRecombinant Fusion ProteinsRecurrenceRegenerationSolubilityTransduction, GeneticTransfectionTunica IntimaVascular Endothelial Growth Factor AWound Healing