ArticleDevelopment (Cambridge, England)2013
miR-21 represses Pdcd4 during cardiac valvulogenesis.
Article in Development (Cambridge, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024Review
- Deciphering sex-specific miRNAs as heat-recorders in zebrafish.Scientific reports · 2022Article
- Insights into role of microRNAs in cardiac development, cardiac diseases, and developing novel therapies.Iranian journal of basic medical sciences · 2020Review
- Inhibition of miR-153 ameliorates ischemia/reperfusion-induced cardiomyocytes apoptosis by regulating Nrf2/HO-1 signaling in rats.Biomedical engineering online · 2020Article
- Role of Programmed Cell Death 4 (PDCD4)-Mediated Akt Signaling Pathway in Vascular Endothelial Cell Injury Caused by Lower-Extremity Ischemia-Reperfusion in Rats.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Quantitative Proteomics Analysis Reveals Novel Targets of miR-21 in Zebrafish Embryos.Scientific reports · 2017Article
- MicroRNA Expression Signature in Human Calcific Aortic Valve Disease.BioMed research international · 2017Article
- Mutations in DCHS1 cause mitral valve prolapse.Nature · 2015Article
- Small molecules, big effects: the role of microRNAs in regulation of cardiomyocyte death.Cell death & disease · 2014Review
- The zebrafish as a tool to identify novel therapies for human cardiovascular disease.Disease models & mechanisms · 2014Review
- Atheroprotective pulsatile flow induces ubiquitin-proteasome-mediated degradation of programmed cell death 4 in endothelial cells.PloS one · 2014Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
The discovery of small non-coding microRNAs has revealed novel mechanisms of post-translational regulation of gene expression, the implications of which are still incompletely understood. We focused on microRNA 21 (miR-21), which is expressed in cardiac valve endothelium during development, in order to better understand its mechanistic role in cardiac valve development. Using a combination of in vivo gene knockdown in zebrafish and in vitro assays in human cells, we show that miR-21 is necessary for proper development of the atrioventricular valve (AV). We identify pdcd4b as a relevant in vivo target of miR-21 and show that protection of pdcd4b from miR-21 binding results in failure of AV development. In vitro experiments using human pulmonic valve endothelial cells demonstrate that miR-21 overexpression augments endothelial cell migration. PDCD4 knockdown alone was sufficient to enhance endothelial cell migration. These results demonstrate that miR-21 plays a necessary role in cardiac valvulogenesis, in large part due to an obligatory downregulation of PDCD4.
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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.