ArticleBiology open2013
The nucleus of endothelial cell as a sensor of blood flow direction.
Article in Biology open, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed.
- Nuclear SUN2 coordinates endothelial cell-matrix interactions to regulate blood vessel homeostasis and barrier function.Angiogenesis · 2026Article
- Copolymers of Poly(Butylene Trans-1,4-Cyclohexanedicarboxylate)/Pripol as New Biomaterial Platform for Small Diameter Vascular Graft.Advanced healthcare materials · 2026Article
- Nuclear SUN2 coordinates endothelial cell-matrix interactions to regulate blood vessel homeostasis and barrier function.bioRxiv : the preprint server for biology · 2026Article
- Development of autologous in vitro vascular models for use in preclinical biotherapeutic development.Blood vessels, thrombosis & hemostasis · 2026Article
- Modeling smooth muscle cell-endothelial cell crosstalk in abdominal aortic aneurysms using 3D microvessels on-chip.Vascular biology (Bristol, England) · 2026Article
- Linking Planar Cell Polarity to Mechanotransduction During Morphogenesis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Nuclear envelope components in vascular mechanotransduction: emerging roles in vascular health and disease.Nucleus (Austin, Tex.) · 2025Review
- Vessel-on-a-Chip to Study Vascular Endothelial Inflammation.Current protocols · 2025Article
- P300 Modulates Endothelial Mechanotransduction of Fluid Shear Stress.Cellular and molecular bioengineering · 2024Article
- Shear Stress and Sub-Femtomolar Levels of Ligand Synergize to Activate ALK1 Signaling in Endothelial Cells.Cells · 2024Article
- Pannexin-3 stabilizes the transcription factor Bcl6 in a channel-independent manner to protect against vascular oxidative stress.Science signaling · 2024Article
- Life at the crossroads: the nuclear LINC complex and vascular mechanotransduction.Frontiers in physiology · 2024Review
- Mechanotransduction of the vasculature in Hutchinson-Gilford Progeria Syndrome.Frontiers in physiology · 2024Review
- Shear Stress and Endothelial Mechanotransduction in Trauma Patients with Hemorrhagic Shock: Hidden Coagulopathy Pathways and Novel Therapeutic Strategies.International journal of molecular sciences · 2023Review
- Nuclear mechanosensing of the aortic endothelium in health and disease.Disease models & mechanisms · 2023Review
- Oscillatory shear stress-induced downregulation of TET1s injures vascular endothelial planar cell polarity by suppression of actin polymerization.APL bioengineering · 2023Article
- Nucleus Mechanosensing in Cardiomyocytes.International journal of molecular sciences · 2023Review
- Engineered Human Tissue as A New Platform for Mosquito Bite-Site Biology Investigations.Insects · 2023Article
- Microfluidic platform for the reproduction of hypoxic vascular microenvironments.Scientific reports · 2023Article
- Nuclear SUN1 stabilizes endothelial cell junctions via microtubules to regulate blood vessel formation.eLife · 2023Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Hemodynamic shear stresses cause endothelial cells (ECs) to polarize in the plane of the flow. Paradoxically, under strong shear flows, ECs disassemble their primary cilia, common sensors of shear, and thus must use an alternative mechanism of sensing the strength and direction of flow. In our experiments in microfluidic perfusion chambers, confluent ECs developed planar cell polarity at a rate proportional to the shear stress. The location of Golgi apparatus and microtubule organizing center was biased to the upstream side of the nucleus, i.e. the ECs polarized against the flow. These in vitro results agreed with observations in murine blood vessels, where EC polarization against the flow was stronger in high flow arteries than in veins. Once established, flow-induced polarization persisted over long time intervals without external shear. Transient destabilization of acto-myosin cytoskeleton by inhibition of myosin II or depolymerization of actin promoted polarization of EC against the flow, indicating that an intact acto-myosin cytoskeleton resists flow-induced polarization. These results suggested that polarization was induced by mechanical displacement of EC nuclei downstream under the hydrodynamic drag. This hypothesis was confirmed by the observation that acute application of a large hydrodynamic force to ECs resulted in an immediate downstream displacement of nuclei and was sufficient to induce persistent polarization. Taken together, our data indicate that ECs can sense the direction and strength of blood flow through the hydrodynamic drag applied to their nuclei.
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Registered trials
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