system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, RESULTS. Meshes: Animals, Aorta, Apolipoproteins E, Arteriosclerosis, Chemokine CCL2, Chemotaxis, Disease Models, Animal, Disease Progression, Genetic Therapy, Humans, Leukocyte Count, Lipids, Mice, Mice, Inbred C57BL, Mice, Knockout, Monocytes, Muscle, Skeletal, Peptide Fragments, Recombinant Proteins, Sequence Deletion, Skin, Transfection, Treatment Outcome.
user
Does new anti-monocyte chemoattractant protein-1 gene therapy attenuate atherosclerosis in apolipoprotein E-knockout mice? Context: 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. 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.
assistant
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. Final Decision: yes