ArticleArteriosclerosis, thrombosis, and vascular biology2018
Shear Stress and VE-Cadherin.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 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
24 citing papers in PubMed, 38 citations in OpenAlex.
- Trimethylamine N-oxide (TMAO) disrupts endothelial junction integrity through VE-cadherin Tyr658 phosphorylation in vitro.Archives of toxicology · 2026Article
- Progress in recapitulating morphogenesis of blood microvascular structures for microphysiological systems development.Biochemical Society transactions · 2025Article
- Reversal of cerebrovascular anomalies in a zebrafish model of vein of Galen aneurysm.Nature cardiovascular research · 2025Article
- Metaboloepigenetics: Role in the Regulation of Flow-Mediated Endothelial (Dys)Function and Atherosclerosis.Cells · 2025Review
- Monocyte-Derived cxcl12 Guides a Directional Migration of Blood Vessels in Zebrafish.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- c-Src-induced vascular malformations require localised matrix degradation at focal adhesions.Journal of cell science · 2024Article
- Flow-induced reprogramming of endothelial cells in atherosclerosis.Nature reviews. Cardiology · 2023Review
- Acetate controls endothelial-to-mesenchymal transition.Cell metabolism · 2023Article
- The role of blood flow in vessel remodeling and its regulatory mechanism during developmental angiogenesis.Cellular and molecular life sciences : CMLS · 2023Review
- Shear stress control of vascular leaks and atheromas through Tie2 activation by VE-PTP sequestration.EMBO molecular medicine · 2023Article
- Impact of spatial and temporal stability of flow vortices on vascular endothelial cells.Biomechanics and modeling in mechanobiology · 2023Article
- The short-chain fatty acid butyrate exerts a specific effect on VE-cadherin phosphorylation and alters the integrity of aortic endothelial cells.Frontiers in cell and developmental biology · 2023Article
- Tyrosine-protein kinase Yes controls endothelial junctional plasticity and barrier integrity by regulating VE-cadherin phosphorylation and endocytosis.Nature cardiovascular research · 2022Article
- Bonding of Flexible Membranes for Perfusable Vascularized Networks Patch.Tissue engineering and regenerative medicine · 2022Article
- On coalescent angiogenesis and the remarkable flexibility of blood vessels.Angiogenesis · 2022Article
- Coalescent angiogenesis-evidence for a novel concept of vascular network maturation.Angiogenesis · 2022Article
- Rictor maintains endothelial integrity under shear stress.Frontiers in cell and developmental biology · 2022Article
- Endothelial Mechanosensors for Atheroprone and Atheroprotective Shear Stress Signals.Journal of inflammation research · 2022Review
- Article
- Vessel Enlargement in Development and Pathophysiology.Frontiers in physiology · 2021Review
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective- Vascular fusion represents an important mechanism of vessel enlargement during development; however, its significance in postnatal vessel enlargement is still unknown. During fusion, 2 adjoining vessels merge to share 1 larger lumen. The aim of this research was to identify the molecular mechanism responsible for vascular fusion. Approach and Results- We previously showed that both low shear stress and DAPT ( N-[ N-(3,5-difluorophenacetyl)-L-alanyl]- S-phenylglycine t-butyl ester) treatment in the embryo result in a hyperfused vascular plexus and that increasing shear stress levels could prevent DAPT-induced fusion. We, therefore, investigated vascular endothelial-cadherin (VEC) phosphorylation because this is a common downstream target of low shear stress and DAPT treatment. VEC phosphorylation increases after DAPT treatment and decreased shear stress. The increased phosphorylation occurred independent of the cleavage of the Notch intracellular domain. Increasing shear stress rescues hyperfusion by DAPT treatment by causing the association of the phosphatase vascular endothelial-protein tyrosine phosphatase with VEC, counteracting VEC phosphorylation. Finally, Src (proto-oncogene tyrosine-protein kinase Src) inhibition prevents VEC phosphorylation in endothelial cells and can rescue hyperfusion induced by low shear stress and DAPT treatment. Moesin, a VEC target that was previously reported to mediate endothelial cell rearrangement during lumenization, relocalizes to cell membranes in vascular beds undergoing hyperfusion. Conclusions- This study provides the first evidence that VEC phosphorylation, induced by DAPT treatment and low shear stress, is involved in the process of fusion during vascular remodeling.
Indexed as
Identifiers
What 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.