ArticleCirculation2009
Regulation of vascular contractility and blood pressure by the E2F2 transcription factor.
Article in Circulation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 30 citations in OpenAlex.
- A non-enzymatic function of neuraminidase 1 restrains hepatic glucagon response in mice.Nature communications · 2026Article
- E2F2 Reprograms Macrophage Function By Modulating Material and Energy Metabolism in the Progression of Metabolic Dysfunction-Associated Steatohepatitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Sam68 is a druggable vulnerability point in cancer stem cells.Cancer metastasis reviews · 2024Review
- Hepatic Sam68 Regulates Systemic Glucose Homeostasis and Insulin Sensitivity.International journal of molecular sciences · 2022Article
- Article
- Identification of key molecular markers of acute coronary syndrome using peripheral blood transcriptome sequencing analysis and mRNA-lncRNA co-expression network construction.Bioengineered · 2021Article
- Ablation of Sam68 in adult mice increases thermogenesis and energy expenditure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Sam68 promotes hepatic gluconeogenesis via CRTC2.Nature communications · 2021Article
- Genetic Variants in Transcription Factor Binding Sites in Humans: Triggered by Natural Selection and Triggers of Diseases.International journal of molecular sciences · 2021Review
- Ablation of lncRNATheranostics · 2021Article
- Resveratrol Attenuates High Glucose-Induced Vascular Endothelial Cell Injury by Activating the E2F3 Pathway.BioMed research international · 2020Article
- Sam68 impedes the recovery of arterial injury by augmenting inflammatory response.Journal of molecular and cellular cardiology · 2019Article
- Gene Expression Profiles Controlled by the Alternative Splicing Factor Nova2 in Endothelial Cells.Cells · 2019Article
- Inhibition of Sam68 triggers adipose tissue browning.The Journal of endocrinology · 2015Article
- Src Family Kinases (SFK) Mediate Angiotensin II-Induced Myosin Light Chain Phosphorylation and Hypertension.PloS one · 2015Article
- E2F1 suppresses cardiac neovascularization by down-regulating VEGF and PlGF expression.Cardiovascular research · 2014Article
- Contrasting roles of E2F2 and E2F3 in endothelial cell growth and ischemic angiogenesis.Journal of molecular and cellular cardiology · 2013Article
- Article
- Rosuvastatin enhances angiogenesis via eNOS-dependent mobilization of endothelial progenitor cells.PloS one · 2013Article
- E2F and microRNA regulation of angiogenesis.American journal of cardiovascular disease · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundRecent studies have identified a polymorphism in the endothelin-converting enzyme (ECE)-1b promoter (-338C/A) that is strongly associated with hypertension in women. The polymorphism is located in a consensus binding sequence for the E2F family of transcription factors. E2F proteins are crucially involved in cell-cycle regulation, but their roles in cardiovascular function are poorly understood. Here, we investigated the potential role of E2F2 in blood pressure regulation. METHODS AND
resultsTail-cuff measurements of systolic and diastolic blood pressures were significantly higher in E2F2-null (E2F2(-/-)) mice than in their wild-type littermates, and in ex vivo ring assays, aortas from the E2F2(-/-) mice exhibited significantly greater contractility in response to big endothelin-1. Big endothelin-1 is activated by ECE-1, and mRNA levels of ECE-1b, the repressive ECE-1 isoform, were significantly lower in E2F2(-/-) mice than in wild-type mice. In endothelial cells, chromatin immunoprecipitation assays confirmed that E2F2 binds the ECE-1b promoter, and promoter-reporter assays indicated that E2F2 activates ECE-1b transcription. Furthermore, loss or downregulation of E2F2 led to a decline in ECE-1b levels, to higher levels of the membranous ECE-1 isoforms (ie, ECE-1a, -1c, and -1d), and to deregulated ECE-1 activity. Finally, Sam68 coimmunoprecipitated with E2F2, occupied the ECE-1b promoter (chromatin immunoprecipitation), and repressed E2F2-mediated ECE-1b promoter activity (promoter-reporter assays).
conclusionsOur results identify a cell-cycle-independent mechanism by which E2F2 regulates endothelial function, arterial contractility, and blood pressure.
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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.