Abstract
Intimal hyperplasia represents a complex pathologic vascular response to injury. Our group previously identified several candidate genes associated with this response. Following implantation of interpositional prosthetic grafts in canine carotid arteries, thrombospondin-2 (TSP-2) was consistently found to be upregulated in the intimal hyperplastic lesion occurring at the anastomosis at 7-, 14-, and 30-day periods. Thus, we sought to determine whether silencing of this gene could attenuate the response to injury and reduce neointima formation in an in vivo model.
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