ArticleFrontiers in physiology2021
Notch Ligand Delta-Like 1 Is Associated With Loss of Vascular Endothelial Barrier Function.
Article in Frontiers in physiology, 2021. 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, 25 citations in OpenAlex.
- Endothelial dysfunction: A central mechanism linking autosomal dominant polycystic kidney disease and intracranial aneurysms (Review).International journal of molecular medicine · 2026Review
- From bench to triage: diagnostic utility of delta-like canonical notch ligand-1 (DLL-1) for early sepsis prediction in the emergency department.Infection · 2026Article
- Evaluating the diagnostic and prognostic utility of serum DLL1 in acute-on-chronic liver failure patients with bacterial infections.Frontiers in medicine · 2026Article
- Soluble DLL1 as an Indicator of acute kidney injury and postoperative delirium following cardiac surgery: a secondary analysis of a prospective study.Perioperative medicine (London, England) · 2025Article
- Association of elevated Delta-like canonical Notch ligand 1 levels with clinical outcomes in patients hospitalized for SARS-CoV2 infection.Scientific reports · 2025Observational
- Multifaceted Role of Notch Signaling in Vascular Health and Diseases.Biomedicines · 2025Review
- Lentinan's effect on gut microbiota and inflammatory cytokines in 5-FU-induced mucositis mice.AMB Express · 2025Article
- RECK as a Potential Crucial Molecule for the Targeted Treatment of Sepsis.Journal of inflammation research · 2025Review
- Barrier genes are associated with preterm birth.Frontiers in medicine · 2025Article
- Notch transcriptional target tmtc1 maintains vascular homeostasis.Cellular and molecular life sciences : CMLS · 2024Article
- Canonical notch activation in patients with scrub typhus: association with organ dysfunction and poor outcome.Infection · 2024Article
- Vascular endothelial dysfunction induced by 3-bromofluoranthene via MAPK-mediated-NFκB pro-inflammatory pathway and intracellular ROS generation.Archives of toxicology · 2024Article
- Evaluation of the Novel Sepsis Biomarker Host-Derived Delta-like Canonical Notch Ligand 1-A Secondary Analysis of 405 Patients Suffering from Inflammatory or Infectious Diseases.International journal of molecular sciences · 2023Article
- ADAM10-a "multitasker" in sepsis: focus on its posttranslational target.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Notch Signaling in Acute Inflammation and Sepsis.International journal of molecular sciences · 2023Review
- Delta-like canonical Notch ligand 1 is predictive for sepsis and acute kidney injury in surgical intensive care patients.Scientific reports · 2022Observational
- Cefiderocol Protects against Cytokine- and Endotoxin-Induced Disruption of Vascular Endothelial Cell Integrity in an In Vitro Experimental Model.Antibiotics (Basel, Switzerland) · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular leakage associated with vascular endothelial cell (vEC) dysfunction is a hallmark of sepsis. Causative for the decreased integrity of the vascular endothelium (vE) is a complex concurrence of pathogen components, inflammation-associated host factors, and the interaction of vECs and activated circulating immune cells. One signaling pathway that regulates the integrity of the vE is the Notch cascade, which is activated through the binding of a Notch ligand to its respective Notch receptor. Recently, we showed that the soluble form of the Notch ligand Delta-like1 (sDLL1) is highly abundant in the blood of patients with sepsis. However, a direct connection between DLL1-activated Notch signaling and loss of vEC barrier function has not been addressed so far. To study the impact of infection-associated sDLL1, we used human umbilical vein cells (HUVEC) grown in a transwell system and cocultured with blood. Stimulation with sDLL1 induced activation as well as loss of endothelial tight structure and barrier function. Moreover, LPS-stimulated HUVEC activation and increase in endothelial cell permeability could be significantly decreased by blocking DLL1-receptor binding and Notch signaling, confirming the involvement of the cascade in LPS-mediated endothelial dysfunction. In conclusion, our results suggest that during bacterial infection and LPS recognition, DLL1-activated Notch signaling is associated with vascular permeability. This finding might be of clinical relevance in terms of preventing vascular leakage and the severity of sepsis.
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