ArticleScientific reports2016
Gene silencing of endothelial von Willebrand Factor attenuates angiotensin II-induced endothelin-1 expression in porcine aortic endothelial cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.
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Who cites it
30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.
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- Circulating Proteomics and Risk of Atrial Fibrillation: A Systematic Review of Cohort Studies.Journal of cellular and molecular medicine · 2025Pooled it
- Endothelial glycocalyx perturbation in obstructive sleep apnea is associated with repetitive hypoxemia and immunothrombotic endothelial dysfunction.Journal of translational medicine · 2026Article
- Galectin-3 binding protein is upregulated in heart failure with preserved ejection fraction and associated with endothelial nitric oxide synthase deficiency.GeroScience · 2026Article
- Integrated Network Pharmacology, Single-Cell Transcriptomics Unveil the Mechanistic Role of Morusin in Aortic Dissection.Journal of cellular and molecular medicine · 2026Article
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- Effects of nicorandil on inflammatory response, oxidative stress and myocardial fibrosis after myocardial infarction.BMC cardiovascular disorders · 2025Article
- From cardiac injury to omics signatures: a narrative review on biomarkers in septic cardiomyopathy.Clinical and experimental medicine · 2025Review
- The impaired white-matter structural network mediates the relationship between the glymphatic system and emotional abnormalities in patients with chronic kidney disease.Quantitative imaging in medicine and surgery · 2025Article
- Unveiling the Angiogenic Potential and Functional Decline of Valve Interstitial Cells During Calcific Aortic Valve Stenosis Progression.Journal of cellular and molecular medicine · 2025Article
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- Small molecule probes for peroxynitrite detection.Redox biochemistry and chemistry · 2024Article
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- Cognitive Impairment in Chronic Kidney Disease Is Associated with Glymphatic System Dysfunction.Kidney diseases (Basel, Switzerland) · 2023Article
- Macrophage-derived exosomal miR-4532 promotes endothelial cells injury by targeting SP1 and NF-κB P65 signalling activation.Journal of cellular and molecular medicine · 2022Article
- An insight into the mechanisms of COVID-19, SARS-CoV2 infection severity concerning β-cell survival and cardiovascular conditions in diabetic patients.Molecular and cellular biochemistry · 2022Review
- GJD Modulates Cardiac/Vascular Inflammation and Decreases Blood Pressure in Hypertensive Rats.Mediators of inflammation · 2022Article
- Angiotensin-converting enzyme 2: a double-edged sword in COVID-19 patients with an increased risk of heart failure.Heart failure reviews · 2021Review
- Neuregulin-1 alleviate oxidative stress and mitigate inflammation by suppressing NOX4 and NLRP3/caspase-1 in myocardial ischaemia-reperfusion injury.Journal of cellular and molecular medicine · 2021Article
- Purinergic Regulation of Endothelial Barrier Function.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of endothelin (ET)-1 is increased in endothelial cells exposed to angiotensin II (Ang II), leading to endothelial dysfunction and cardiovascular disorders. Since von Willebrand Factor (vWF) blockade improves endothelial function in coronary patients, we hypothesized that targeting endothelial vWF with short interference RNA (siRNA) prevents Ang II-induced ET-1 upregulation. Nearly 65 ± 2% silencing of vWF in porcine aortic endothelial cells (PAOECs) was achieved with vWF-specific siRNA without affecting cell viability and growth. While showing ET-1 similar to wild type cells at rest, vWF-silenced cells did not present ET-1 upregulation during exposure to Ang II (100 nM/24 h), preserving levels of endothelial nitric oxide synthase activity similar to wild type. vWF silencing prevented AngII-induced increase in nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) activity and superoxide anion (O2-) levels, known triggers of ET-1 expression. Moreover, no increase in O2- or ET-1 levels was found in silenced cells treated with AngII or NOX-agonist phorbol ester (PMA 5 nM/48 h). Finally, vWF was required for overexpression of NOX4 and NOX2 in response to AngII and PMA. In conclusion, endothelial vWF knockdown prevented Ang II-induced ET-1 upregulation through attenuation of NOX-mediated O2- production. Our findings reveal a new role of vWF in preventing of Ang II-induced endothelial dysfunction.
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