再狭窄
新生内膜增生
医学
血管平滑肌
新生内膜
外膜
癌症研究
病理
内科学
支架
心脏病学
平滑肌
作者
Eléonore M'Baya-Moutoula,Alexandre Marchand,Isabelle Six,Noura Bahrar,Tanja Ćelić,Nathalie Mougenot,Pierre Maitrias,Ziad A. Massy,Anne‐Marie Lompré,Laurent Metzinger,Valérie Metzinger-Le Meuth
出处
期刊:Current Vascular Pharmacology
[Bentham Science]
日期:2020-08-10
卷期号:18 (5): 507-516
被引量:9
标识
DOI:10.2174/1570161117666190705141152
摘要
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 injury. 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. Conclusions: Down-regulating miR-223 could be a potential therapeutic approach to prevent restenosis after angioplasty.
科研通智能强力驱动
Strongly Powered by AbleSci AI