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

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Abstract

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.

Original languageEnglish
Pages (from-to)1273-1282
Number of pages10
JournalGene Therapy
Volume11
Issue number16
DOIs
Publication statusPublished - Aug 2004

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Molecular Biology
  • Genetics

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    Ohtani, K., Usui, M., Nakano, K., Kohjimoto, Y., Kitajima, S., Hirouchi, Y., Li, X. H., Kitamoto, S., Takeshita, A., & Egashira, K. (2004). Antimonocyte chemoattractant protein-1 gene therapy reduces experimental in-stent restenosis in hypercholesterolemic rabbits and monkeys. Gene Therapy, 11(16), 1273-1282. https://doi.org/10.1038/sj.gt.3302288