Blockade of vascular endothelial growth factor suppresses experimental restenosis after intraluminal injury by inhibiting recruitment of monocyte lineage cells

Kisho Ohtani, Kensuke Egashira, Ken Ichi Hiasa, Qingwei Zhao, Shiro Kitamoto, Minako Ishibashi, Makoto Usui, Shujiro Inoue, Yoshikazu Yonemitsu, Katsuo Sueishi, Masataka Sata, Masabumi Shibuya, Kenji Sunagawa

Research output: Contribution to journalArticle

111 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)2444-2452
Number of pages9
JournalCirculation
Volume110
Issue number16
DOIs
Publication statusPublished - Oct 19 2004

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Vascular Endothelial Growth Factor A
Monocytes
Wounds and Injuries
Genes
Vascular Endothelial Growth Factor Receptor-1
Adventitia
Chemokine CCL2
Vascular System Injuries
Blood Vessels
Rabbits
Inflammation

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Blockade of vascular endothelial growth factor suppresses experimental restenosis after intraluminal injury by inhibiting recruitment of monocyte lineage cells. / 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.

In: Circulation, Vol. 110, No. 16, 19.10.2004, p. 2444-2452.

Research output: Contribution to journalArticle

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. / Blockade of vascular endothelial growth factor suppresses experimental restenosis after intraluminal injury by inhibiting recruitment of monocyte lineage cells. In: Circulation. 2004 ; Vol. 110, No. 16. pp. 2444-2452.
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AU - Hiasa, Ken Ichi

AU - Zhao, Qingwei

AU - Kitamoto, Shiro

AU - Ishibashi, Minako

AU - Usui, Makoto

AU - Inoue, Shujiro

AU - Yonemitsu, Yoshikazu

AU - Sueishi, Katsuo

AU - Sata, Masataka

AU - Shibuya, Masabumi

AU - Sunagawa, Kenji

PY - 2004/10/19

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N2 - 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.

AB - 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.

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