ArticleCell research2013
Hypertensive stretch regulates endothelial exocytosis of Weibel-Palade bodies through VEGF receptor 2 signaling pathways.
Article in Cell research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 37 citations in OpenAlex.
- Immunology of Normal Pregnancy and Preeclampsia and the Role of Placental Non-Classical HLA and Decidual NK Cells.International journal of molecular sciences · 2026Review
- Article
- Uniaxial cyclic stretch regulates the expression of thrombomodulin and von Willebrand factor on endothelial cells.Blood vessels, thrombosis & hemostasis · 2025Article
- Loss of pulsatility with continuous-flow left ventricular assist devices and the significance of the arterial endothelium in von-Willebrand factor production and degradation.Artificial organs · 2023Review
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Systems Biology Analysis of Temporal Dynamics That Govern Endothelial Response to Cyclic Stretch.Biomolecules · 2022Review
- Hypertension meets osteoarthritis - revisiting the vascular aetiology hypothesis.Nature reviews. Rheumatology · 2021Review
- BRAF Modulates Stretch-Induced Intercellular Gap Formation through Localized Actin Reorganization.International journal of molecular sciences · 2021Article
- High intraluminal pressure promotes vascular inflammation via caveolin-1.Scientific reports · 2021Article
- The potential roles of Von Willebrand factor and neutrophil extracellular traps in the natural history of hypertrophic and hypertensive cardiomyopathy.Thrombosis research · 2020Review
- Acquired von Willebrand Syndrome in Patients With Ventricular Assist Device.Frontiers in medicine · 2019Review
- Gasotransmitter Heterocellular Signaling.Antioxidants & redox signaling · 2017Article
- Advances in on-chip vascularization.Regenerative medicine · 2017Review
- Static mechanical strain induces capillary endothelial cell cycle re-entry and sprouting.Physical biology · 2016Article
- Mechanical stretch: physiological and pathological implications for human vascular endothelial cells.Vascular cell · 2015Review
- High matrix metalloproteinase-9 expression induces angiogenesis and basement membrane degradation in stroke-prone spontaneously hypertensive rats after cerebral infarction.Neural regeneration research · 2014Article
- Acute mechanical stretch promotes eNOS activation in venous endothelial cells mainly via PKA and Akt pathways.PloS one · 2013Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulated endothelial exocytosis of Weibel-Palade bodies (WPBs), the first stage in leukocyte trafficking, plays a pivotal role in inflammation and injury. Acute mechanical stretch has been closely associated with vascular inflammation, although the precise mechanism is unknown. Here, we show that hypertensive stretch regulates the exocytosis of WPBs of endothelial cells (ECs) through VEGF receptor 2 (VEGFR2) signaling pathways. Stretch triggers a rapid release (within minutes) of von Willebrand factor and interleukin-8 from WPBs in cultured human ECs, promoting the interaction between leukocytes and ECs through the translocation of P-selectin to the cell membrane. We further show that hypertensive stretch significantly induces P-selectin translocation of intact ECs and enhances leukocyte adhesion both ex vivo and in vivo. Stretch-induced endothelial exocytosis is mediated via a VEGFR2/PLCγ1/calcium pathway. Interestingly, stretch also induces a negative feedback via a VEGFR2/Akt/nitric oxide pathway. Such dual effects are confirmed using pharmacological and genetic approaches in carotid artery segments, as well as in acute hypertensive mouse models. These studies reveal mechanical stretch as a potent agonist for endothelial exocytosis, which is modulated by VEGFR2 signaling. Thus, VEGFR2 signaling pathways may represent novel therapeutic targets in limiting hypertensive stretch-related inflammation.
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