Objective: Restenosis is a frequent complication of angioplasty. It consists of a neointimal
hyperplasia resulting from progression and migration of vascular smooth muscle cells (VSMC) into the
vessel lumen. microRNA miR-223 has recently been shown to be involved in cardiovascular diseases
including atherosclerosis, vascular calcification and arterial thrombosis. In this study, our aim was to
assess the impact of miR-223 modulation on restenosis in a rat model of carotid artery after balloon
Methods: The over and down-expression of miR-223 was induced by adenoviral vectors, containing
either a pre-miR-223 sequence allowing artificial miR-223 expression or a sponge sequence, trapping
the native microRNA, respectively. Restenosis was quantified on stained rat carotid sections.
Results: In vitro, three mRNA (Myocyte Enhancer Factor 2C (MEF2C), Ras homolog gene family,
member B (RhoB) and Nuclear factor 1 A-type (NFIA)) reported as miR-223 direct targets and known
to be implicated in VSMC differentiation and contractility were studied by RT-qPCR. Our findings
showed that down-expression of miR-223 significantly reduced neointimal hyperplasia by 44% in carotids,
and was associated with a 2-3-fold overexpression of MEF2C, RhoB and NFIA in a murine monocyte
macrophage cell line, RAW 264.7 cells.
Conclusion: Down-regulating miR-223 could be a potential therapeutic approach to prevent restenosis