ArticleAmerican journal of translational research2019
Linc-POU3F3 is overexpressed in in-stent restenosis patients and induces VSMC phenotypic transformation via POU3F3/miR-449a/KLF4 signaling pathway.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Exosomal ncRNAs in liquid biopsy: a new paradigm for early cancer diagnosis and monitoring.Frontiers in oncology · 2025Review
- Noncoding RNAs in Vascular Cell Biology and Restenosis.Biology · 2022Review
- Circular RNA circUBR4 regulates ox-LDL-induced proliferation and migration of vascular smooth muscle cells through miR-185-5p/FRS2 axis.Molecular and cellular biochemistry · 2021Article
- Roles of MicroRNAs in Peripheral Artery In-Stent Restenosis after Endovascular Treatment.BioMed research international · 2021Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWith the extensive application of stent implantation in patients undergoing percutaneous coronary interventions (PCI), there are chances that in-stent restenosis (ISR)-a major vascular complication caused by vascular smooth muscle cell (VSMC) phenotypic transformation-might occur.
objectivesThis study sought to evaluate the role of lincRNA-POU3F3 on VSMC phenotypic transformation and the underlying mechanism.
methodsVSMCs were used in our research. We first constructed a gene delivery system through an assembly of lipofectamine and a functional plasmid DNA (pDNA) encoding lincRNA-POU3F3 or MicroRNA-449a, and then, transfected it to VSMCs. Moreover, lentivirus-mediated KLF4 inhibitor (KLF4 siRNA) was also used in these cells. Expression of relevant proteins, such as smooth muscle myosin heavy chain (SM-MHC), alpha smooth muscle actin (α-SMA), osteopontin (OPN), and kruppel-like factor 4 (KLF4), was examined by western blot or immunofluorescence (IF) assay. CCK-8 and wound healing assays were performed to assess the growth and migration of VSMCs. qRT-PCR was used to assess linc-POU3F3 and miR-449a levels. Luciferase reporter assay was also performed.
resultsPOU3F3 levels were significantly higher in ISR patients compared to controls. We observed that linc-POU3F3 promoted VSMC proliferation and migration, and induced VSMC phenotypic transformation via POU3F3/miR-449a/KLF4 signaling pathway.
conclusionLinc-POU3F3 promotes phenotypic transformation of VSMCs via POU3F3/miR-449a/KLF4 pathway. It may provide a theoretical basis to attenuate ISR via pharmacological inhibition of this biomarker or at least serve as a predictor of diagnosis or prognosis of patients with restenosis.
Indexed as
Identifiers
31396351PMC6684896W3022731429What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.