Key result
Intramuscular transfer of a mutant MCP-1 gene suppressed monocyte recruitment and vascular medial thickening, but not perivascular fibrosis, in a rat model of NO synthesis blockade.
Why the study?
Does intramuscular transfer of a mutant MCP-1 gene inhibit vascular remodeling in a rat model of chronic NO synthesis blockade?
Population
Rat model in which chronic inhibition of endothelial nitric oxide synthesis induces early vascular…
Design
Preclinical
Authors
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Supports MCP-1 targeting for medial thickening in experimental models; leaves open human translation and perivascular fibrosis effects.
Does intramuscular transfer of a mutant MCP-1 gene inhibit vascular remodeling in a rat model of chronic NO synthesis blockade?
Anti-MCP-1 gene therapy via intramuscular transfer of a mutant gene successfully inhibits monocyte recruitment and vascular medial thickening in a rat model of arteriosclerosis.
Egashira et al. (2000) studied Arteriosclerosis and vascular remodeling. Mutant MCP-1 gene therapy was evaluated on Monocyte recruitment, vascular medial thickening, and perivascular fibrosis. Intramuscular transfer of a mutant MCP-1 gene suppressed monocyte recruitment and vascular medial thickening, but not perivascular fibrosis, in a rat model of NO synthesis blockade.
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