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.
journal_name
Gene Therjournal_title
Gene therapyauthors
Ohtani K,Usui M,Nakano K,Kohjimoto Y,Kitajima S,Hirouchi Y,Li XH,Kitamoto S,Takeshita A,Egashira Kdoi
10.1038/sj.gt.3302288keywords:
subject
Has Abstractpub_date
2004-08-01 00:00:00pages
1273-82issue
16eissn
0969-7128issn
1476-5462pii
3302288journal_volume
11pub_type
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