Key result
AdCMV.hTIMP-2 cuts neointimal area ~53% in injured rat arteries by inhibiting SMC migration.
Why the study?
Does AdCMV.hTIMP-2 gene transfer reduce smooth muscle cell invasiveness and neointimal development in injured rat carotid arteries?
Does AdCMV.hTIMP-2 gene transfer reduce smooth muscle cell invasiveness and neointimal development in injured rat carotid arteries?
Effect estimate: 36% inhibition of SMC migration at 4 days; 53% inhibition of neointimal area at 8 days
p-value: p=<0.05 for 4 days; <0.01 for 8 days
Adenovirus-mediated hTIMP-2 gene transfer delays neointimal development after carotid injury by inhibiting smooth muscle cell invasiveness.
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Supports TIMP-2 gene therapy against restenosis; leaves open translation from rat carotid injury to clinical use.
Cheng et al. (1998) studied Endovascular injury and neointimal development. Adenovirus carrying cDNA for human tissue inhibitor of metalloproteinase-2 (AdCMV.hTIMP-2) vs. Control virus (AdCMV.null or AdCMV.betagal) was evaluated on Smooth muscle cell migration into the intima and neointimal area (36% inhibition of SMC migration at 4 days; 53% inhibition of neointimal area at 8 days, p=<0.05 for 4 days; <0.01 for 8 days). Delivery of AdCMV.hTIMP-2 to the injured rat carotid artery inhibited SMC migration into the intima by 36% at 4 days (P<0.05) and reduced neointimal area by 53% at 8 days (P<0.01).
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