Antimonocyte chemoattractant protein-1 gene therapy reduces experimental in-stent restenosis in hypercholesterolemic rabbits and monkeys

K. Ohtani, M. Usui, K. Nakano, Y. Kohjimoto, S. Kitajima, Y. Hirouchi, X. H. Li, S. Kitamoto, A. Takeshita, K. Egashira

研究成果: ジャーナルへの寄稿学術誌査読

47 被引用数 (Scopus)

抄録

In-stent restenosis results exclusively from neointimal hyperplasia due to mechanical injury and a foreign body response to the prosthesis. Inflammation mediated by monocyte chemoattractant protein-1 (MCP-1) might therefore underlie in-stent restenosis. We recently devised a new strategy for anti-MCP-1 gene therapy by transfecting an N-terminal deletion mutant of the MCP-1 gene into skeletal muscles. We used this strategy to investigate the role of MCP-1 in experimental in-stent restenosis in hypercholesterolemic rabbits and monkeys. Transfection of the mutant MCP-1 gene suppressed monocyte infiltration/activation in the stented arterial wall and markedly reduced the development of neointimal hyperplasia. This strategy also suppressed local expression of MCP-1 and inflammatory cytokines. Therefore, inhibition of MCP-1-mediated inflammation is effective in reducing experimental in-stent restenosis. This strategy might be a useful form of gene therapy against human in-stent restenosis.

本文言語英語
ページ(範囲)1273-1282
ページ数10
ジャーナルGene Therapy
11
16
DOI
出版ステータス出版済み - 8月 2004
外部発表はい

!!!All Science Journal Classification (ASJC) codes

  • 分子医療
  • 分子生物学
  • 遺伝学

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