ArticleCurrent biology : CB2013
Fluid shear stress on endothelial cells modulates mechanical tension across VE-cadherin and PECAM-1.
Article in Current biology : CB, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 301 papers.
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Who cites it
301 citing papers in PubMed, 500 citations in OpenAlex.
- Loss of Smad4 drives vascular malformations via c-KIT-dependent high-fluid shear stress mimicry.The Journal of clinical investigation · 2026Article
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- Mechanosensitive FHL2 tunes endothelial function via microtubule-actomyosin crosstalk.The EMBO journal · 2026Article
- Cardiac mechanotransduction from development to disease.APL bioengineering · 2026Review
- Primary Blast-Induced Traumatic Brain Injury as a Risk Factor for (Cerebro)vascular Disorder: Clinical Manifestations, Blast Physics, Biomechanics, Pathobiology, and Critical Gaps.International journal of molecular sciences · 2026Review
- Ultrasound-targeted microbubble cavitation enhances anti-PD-L1 therapy in TNBC via eNOS-mediated reoxygenation.JCI insight · 2026Article
- VE-Cadherin-Actin Regulation Promotes Mechanotransduction and Monolayer Maturation Involving a Tension-Sensitive Intermediate State.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- VE-cadherin interaction proteomics identifies ARVCF as stabilizer of endothelial adherens junctions.iScience · 2026Article
- Micropatterning transcriptionally and phenotypically reprograms endothelial cells.Acta biomaterialia · 2026Article
- Plakoglobin transmits tension across VE-cadherin for vascular leak formation and leukocyte diapedesis.The EMBO journal · 2026Article
- Modular Integration of Impedance Sensing for Real-Time Assessment of Barrier Integrity.bioRxiv : the preprint server for biology · 2026Article
- Oscillatory shear stress-driven endothelial-to-mesenchymal transition: a critical mechanical signal transduction mechanism in atherosclerosis progression.Cell death discovery · 2026Review
- Mechanical states of a motor protein in the spindle.Current biology : CB · 2026Article
- Endothelial Surface Glycocalyx in Vascular Functions and Diseases.Advances in experimental medicine and biology · 2026Review
- Mechanisms of mitral valve development and disease.Frontiers in cardiovascular medicine · 2026Review
- The Fluidic Shear Stress Loading Method Enables Mechanobiological Stimulation in an On-Chip Pump-Integrated Microphysiological System.Micromachines · 2025Article
- Lats1/2 Are Essential for Developmental Vascular Remodeling and Biomechanical Adaptation to Shear Stress.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Mechanobiology of the blood-brain barrier during development, disease and ageing.Nature communications · 2025Review
- Review
241 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Fluid shear stress (FSS) from blood flow acting on the endothelium critically regulates vascular morphogenesis, blood pressure, and atherosclerosis. FSS applied to endothelial cells (ECs) triggers signaling events including opening of ion channels, activation of signaling pathways, and changes in gene expression. Elucidating how ECs sense flow is important for understanding both normal vascular function and disease. EC responses to FSS are mediated in part by a junctional mechanosensory complex consisting of VE-cadherin, PECAM-1, and VEGFR2. Previous work suggested that flow increases force on PECAM-1, which initiates signaling. Deletion of PECAM-1 blocks responses to flow in vitro and flow-dependent vascular remodeling in vivo. To understand this process, we developed and validated FRET-based tension sensors for VE-cadherin and PECAM-1 using our previously developed FRET tension biosensor. FRET measurements showed that in static culture, VE-cadherin in cell-cell junctions bears significant myosin-dependent tension, whereas there was no detectable tension on VE-cadherin outside of junctions. Onset of shear stress triggered a rapid (<30 s) decrease in tension across VE-cadherin, which paralleled a decrease in total cell-cell junctional tension. Flow triggered a simultaneous increase in tension across junctional PECAM-1, while nonjunctional PECAM-1 was unaffected. Tension on PECAM-1 was mediated by flow-stimulated association with vimentin. These data confirm the prediction that shear increases force on PECAM-1. However, they also argue against the current model of passive transfer of force through the cytoskeleton to the junctions, showing instead that flow triggers cytoskeletal remodeling, which alters forces across the junctional receptors.
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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.