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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 
 

New anti- monocyte chemoattractant protein-1 gene therapy attenuates atherosclerosis in apolipoprotein E-knockout mice.

BACKGROUND: Monocyte recruitment into the arterial wall and its activation may be the central event in atherogenesis. Monocyte chemoattractant protein-1 ( MCP-1) is an important chemokine for monocyte recruitment, and its receptor ( CCR2) may mediate such in vivo response. Although the importance of the MCP-1/ CCR2 pathway in atherogenesis has been clarified, it remains unanswered whether postnatal blockade of the MCP-1 signals could be a unique site-specific gene therapy. METHODS AND RESULTS: We devised a new strategy for anti- MCP-1 gene therapy to treat atherosclerosis by transfecting an N-terminal deletion mutant of the human MCP-1 gene into a remote organ (skeletal muscle) in apolipoprotein E-knockout mice. This strategy effectively blocked MCP-1 activity and inhibited the formation of atherosclerotic lesions but had no effect on serum lipid concentrations. Furthermore, this strategy increased the lesional extracellular matrix content. CONCLUSIONS: We conclude that this anti- MCP-1 gene therapy may serve not only to reduce atherogenesis but also to stabilize vulnerable atheromatous plaques. This strategy may be a useful and feasible form of gene therapy against atherosclerosis in humans.[1]

References

  1. New anti-monocyte chemoattractant protein-1 gene therapy attenuates atherosclerosis in apolipoprotein E-knockout mice. Ni, W., Egashira, K., Kitamoto, S., Kataoka, C., Koyanagi, M., Inoue, S., Imaizumi, K., Akiyama, C., Nishida, K.I., Takeshita, A. Circulation (2001) [Pubmed]
 
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