Abstract

INTRODUCTION: Balloon catheter injury causes de-endothelialization and neointimal hyperplasia. Intimal smooth muscle cells (I-SMCs), forming a pseudoendothelium in the endotheliumdenuded vessels, continue to express high levels of adhesive molecules P-selectin and monocyte chemotactic protein-1 (MCP-1) and to recruit mononuclear cells, thus perpetuating the inflammatory response. Since rapamycin, an inhibitor of mammalian target of rapamycin (mTOR), can attenuate inflammation after vascular intervention, we investigated whether rapamycin would affect the proadhesive activity of I-SMCs, which are distinctly different from normal medial SMCs (M-SMCs).

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