ArticleCardiovascular research2019
Identification of atheroprone shear stress responsive regulatory elements in endothelial cells.
Article in Cardiovascular research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 57 citations in OpenAlex.
- Epigenetic regulation in atherosclerosis and its therapeutic potential.Nature reviews. Cardiology · 2026Review
- VE-Cadherin-Actin Regulation Promotes Mechanotransduction and Monolayer Maturation Involving a Tension-Sensitive Intermediate State.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Evidence for Drop-Like Nuclear Deformation in Sheared Endothelial Monolayers.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Article
- Thrombopoietin mimetic reduces mouse lung inflammation and fibrosis after radiation by attenuating activated endothelial phenotypes.JCI insight · 2024Article
- Mechanosensory entities and functionality of endothelial cells.Frontiers in cell and developmental biology · 2024Review
- Moving from lipids to leukocytes: inflammation and immune cells in atherosclerosis.Frontiers in cell and developmental biology · 2024Review
- Early growth response-1, a dynamic conduit in cardiovascular disease.Frontiers in cardiovascular medicine · 2024Review
- Nuclear mechanosensing of the aortic endothelium in health and disease.Disease models & mechanisms · 2023Review
- Fluid shear stress-modulated chromatin accessibility reveals the mechano-dependency of endothelial SMAD1/5-mediated gene transcription.iScience · 2023Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Disturbed flow increases endothelial inflammation and permeability via a Frizzled-4-β-catenin-dependent pathway.Journal of cell science · 2023Article
- Atherosclerosis and endothelial mechanotransduction: current knowledge and models for future research.American journal of physiology. Cell physiology · 2023Review
- Endothelial cell dysfunction in cardiac disease: driver or consequence?Frontiers in cell and developmental biology · 2023Review
- Shear stress regulation of nanoparticle uptake in vascular endothelial cells.Regenerative biomaterials · 2023Review
- Transcriptomic analysis of a 3D blood-brain barrier model exposed to disturbed fluid flow.Fluids and barriers of the CNS · 2022Article
- A single-cell atlas of non-haematopoietic cells in human lymph nodes and lymphoma reveals a landscape of stromal remodelling.Nature cell biology · 2022Article
- Shear stress switches the association of endothelial enhancers from ETV/ETS to KLF transcription factor binding sites.Scientific reports · 2022Article
- Uncovering emergent phenotypes in endothelial cells by clustering of surrogates of cardiovascular risk factors.Scientific reports · 2022Article
- The Induction of Endothelial Autophagy and Its Role in the Development of Atherosclerosis.Frontiers in cardiovascular medicine · 2022Review
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsOscillatory shear stress (OSS) is an atheroprone haemodynamic force that occurs in areas of vessel irregularities and is implicated in the pathogenesis of atherosclerosis. Changes in signalling and transcriptional programme in response to OSS have been vigorously studied; however, the underlying changes in the chromatin landscape controlling transcription remain to be elucidated. Here, we investigated the changes in the regulatory element (RE) landscape of endothelial cells under atheroprone OSS conditions in an in vitro model. METHODS AND
resultsAnalyses of H3K27ac chromatin immunoprecipitation-Seq enrichment and RNA-Seq in primary human umbilical vein endothelial cells 6 h after onset of OSS identified 2806 differential responsive REs and 33 differentially expressed genes compared with control cells kept under static conditions. Furthermore, gene ontology analyses of putative RE-associated genes uncovered enrichment of WNT/HIPPO pathway and cytoskeleton reorganization signatures. Transcription factor (TF) binding motif analysis within RE sequences identified over-representation of ETS, Zinc finger, and activator protein 1 TF families that regulate cell cycle, proliferation, and apoptosis, implicating them in the development of atherosclerosis. Importantly, we confirmed the activation of EGR1 as well as the YAP/TAZ complex early (6 h) after onset of OSS in both cultured human vein and artery endothelial cells and, by undertaking luciferase assays, functionally verified their role in RE activation in response to OSS.
conclusionsBased on the identification and verification of specific responsive REs early upon OSS exposure, we propose an expanded mechanism of how OSS might contribute to the development of atherosclerosis.
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