ArticleThe Journal of biological chemistry2014
Shear stress-induced redistribution of vascular endothelial-protein-tyrosine phosphatase (VE-PTP) in endothelial cells and its role in cell elongation.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Flow transports extracellular lipid-anchored proteins across the surface of living COS-7 cells.Biophysical journal · 2026Article
- Flow transports extracellular lipid-anchored proteins across the surface of living COS-7 cells.bioRxiv : the preprint server for biology · 2025Article
- VE-PTP controls a fluid shear stress set point that governs cell morphological responses through Tie-2.Frontiers in cell and developmental biology · 2025Article
- Resilience to diabetic retinopathy.Progress in retinal and eye research · 2024Review
- HEG1 Protects Against Atherosclerosis by Regulating Stable Flow-Induced KLF2/4 Expression in Endothelial Cells.Circulation · 2024Article
- Heterogeneity of endothelial VE-PTP downstream polarization, Tie2 activation, junctional claudin-5, and permeability in the aorta and vena cava.Cell and tissue research · 2024Article
- Shear stress control of vascular leaks and atheromas through Tie2 activation by VE-PTP sequestration.EMBO molecular medicine · 2023Article
- Heterozygosity for ADP-ribosylation factor 6 suppresses the burden and severity of atherosclerosis.PloS one · 2023Article
- Actin cytoskeleton in angiogenesis.Biology open · 2022Review
- Renal microvascular endothelial cell responses in sepsis-induced acute kidney injury.Nature reviews. Nephrology · 2022Review
- Phosphoproteomic response of cardiac endothelial cells to ischemia and ultrasound.Biochimica et biophysica acta. Proteins and proteomics · 2021Article
- YAP expression in endothelial cells prevents ventilator-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Flow-induced Reorganization of Laminin-integrin Networks Within the Endothelial Basement Membrane Uncovered by Proteomics.Molecular & cellular proteomics : MCP · 2020Article
- To Fuse or Not to Fuse.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Altered DNA methylation indicates an oscillatory flow mediated epithelial-to-mesenchymal transition signature in ascending aorta of patients with bicuspid aortic valve.Scientific reports · 2018Article
- Expression of receptor-type protein tyrosine phosphatase in developing and adult renal vasculature.PloS one · 2017Article
- Angiopoietin-Tie signalling in the cardiovascular and lymphatic systems.Clinical science (London, England : 1979) · 2017Review
- Hemodynamic shear stress via ROS modulates PCSK9 expression in human vascular endothelial and smooth muscle cells and along the mouse aorta.Antioxidants & redox signaling · 2015 · on this mapArticle
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular endothelial cells (ECs) are continuously exposed to shear stress (SS) generated by blood flow. Such stress plays a key role in regulation of various aspects of EC function including cell proliferation and motility as well as changes in cell morphology. Vascular endothelial-protein-tyrosine phosphatase (VE-PTP) is an R3-subtype PTP that possesses multiple fibronectin type III-like domains in its extracellular region and is expressed specifically in ECs. The role of VE-PTP in EC responses to SS has remained unknown, however. Here we show that VE-PTP is diffusely localized in ECs maintained under static culture conditions, whereas it undergoes rapid accumulation at the downstream edge of the cells relative to the direction of flow in response to SS. This redistribution of VE-PTP triggered by SS was found to require its extracellular and transmembrane regions and was promoted by integrin engagement of extracellular matrix ligands. Inhibition of actin polymerization or of Cdc42, Rab5, or Arf6 activities attenuated the SS-induced redistribution of VE-PTP. VE-PTP also underwent endocytosis in the static and SS conditions. SS induced the polarized distribution of internalized VE-PTP. Such an effect was promoted by integrin engagement of fibronectin but prevented by inhibition of Cdc42 activity or of actin polymerization. In addition, depletion of VE-PTP by RNA interference in human umbilical vein ECs blocked cell elongation in the direction of flow induced by SS. Our results suggest that the polarized redistribution of VE-PTP in response to SS plays an important role in the regulation of EC function by blood flow.
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