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pmid: 28063931
Restenosis is mainly attributed to excessive proliferation of vascular smooth muscle cells (VSMCs). Noncoding RNAs have been identified as key regulators of diverse pathological processes. We reported that the long noncoding RNA H19 (LncRNA H19) and LncRNA H19-derived microRNA (miR-675) are overexpressed in neointima of balloon-injured artery. Thus, the present study aims to evaluate the role of LncRNA H19 on VSMCs proliferation. To determine the changes of LncRNA H19 and miR-675 expression in the injured arterial wall, the standard rat carotid artery balloon injury model was used. In vivo studies demonstrated that both LncRNA H19 and miR-675 were upregulated after vascular injury. Correlation analysis revealed a positive relationship between LncRNA H19/miR-675 and the ratio of intima to media. Gain-of-function studies showed that the overexpression of LncRNA H19 accelerated T/G HA-VSMC proliferation in vitro. We further validated that PTEN is the target gene of miR-675 as demonstrated by luciferase assay. Finally, the results of the rescue experiment indicated that LncRNA H19 promoted the proliferation of T/G HA-VSMC in a miR-675-dependent manner. This finding not only reveal a novel function of LncRNA H19, but also has important diagnostic and therapeutic implications in the setting of restenosis and perhaps other vascular proliferative disorders as well.
MicroRNAs, Graft Occlusion, Vascular, PTEN Phosphohydrolase, Animals, RNA, Long Noncoding, Carotid Artery Injuries, Muscle, Smooth, Vascular, Cell Proliferation, Rats
MicroRNAs, Graft Occlusion, Vascular, PTEN Phosphohydrolase, Animals, RNA, Long Noncoding, Carotid Artery Injuries, Muscle, Smooth, Vascular, Cell Proliferation, Rats
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 60 | |
popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Top 10% | |
influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 1% |