We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Antimonocyte chemoattractant protein-1 gene therapy reduces experimental in-stent restenosis in hypercholesterolemic rabbits and monkeys.
- Authors
Ohtani, K.; Usui, M.; Nakano, K.; Kohjimoto, Y.; Kitajima, S.; Hirouchi, Y.; Li, X-H.; Kitamoto, S.; Takeshita, A.; Egashira, K.
- 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.Gene Therapy (2004) 11, 1273-1282. doi:10.1038/sj.gt.3302288 Published online 3 June 2004
- Subjects
MONOCYTES; GENE therapy; SURGICAL stents; CORONARY restenosis; HYPERCHOLESTEREMIA; CYTOKINES; IMMUNOREGULATION
- Publication
Gene Therapy, 2004, Vol 11, Issue 16, p1273
- ISSN
0969-7128
- Publication type
Article
- DOI
10.1038/sj.gt.3302288