ArticleNature communications2016
F-actin-rich contractile endothelial pores prevent vascular leakage during leukocyte diapedesis through local RhoA signalling.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
What it found
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Who cites it
86 citing papers in PubMed, 141 citations in OpenAlex.
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- Role of neutrophils in regulating vascular permeability in inflammatory and autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- CU104, a novel barrier function enhancer, improves colitis via modulation of barrier function and immune cell recruitment.Frontiers in immunology · 2026Article
- Mechanisms That Prevent Vascular Leakage During Leukocyte Extravasation.Acta physiologica (Oxford, England) · 2025Review
- Effects of Non-Cardiac/Non-neurologic Surgery and Anaesthesia on the CSF Proteome, and Modulation by the APOE Mimetic Peptide CN-105.medRxiv : the preprint server for health sciences · 2025Article
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- Advancing Multicolor Super-Resolution Volume Imaging: Illuminating Complex Cellular Dynamics.JACS Au · 2025Review
- Neutrophil extracellular traps-related genes contribute to sepsis-associated acute kidney injury.BMC nephrology · 2025Article
- A specific role for endothelial EPLIN-isoform-regulated actin dynamics in neutrophil transmigration.Scientific reports · 2025Article
- Higher aged neutrophils and differential inflammatory profiles in sickle cell disease patients on chronic transfusion therapy versus those on hydroxyurea.Frontiers in immunology · 2025Article
- Tension at the gate: sensing mechanical forces at the blood-brain barrier in health and disease.Journal of neuroinflammation · 2024Review
- trans-Endothelial neutrophil migration activates bactericidal function via Piezo1 mechanosensing.Immunity · 2024Article
- The senescent secretome drives PLVAP expression in cultured human hepatic endothelial cells to promote monocyte transmigration.iScience · 2023Article
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- Pathological hemodynamic changes and leukocyte transmigration disrupt the blood-spinal cord barrier after spinal cord injury.Journal of neuroinflammation · 2023Article
- Review
- Cell-based optimization and characterization of genetically encoded location-based biosensors for Cdc42 or Rac activity.Journal of cell science · 2023Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 5 countries.
Funding
Abstract
During immune surveillance and inflammation, leukocytes exit the vasculature through transient openings in the endothelium without causing plasma leakage. However, the exact mechanisms behind this intriguing phenomenon are still unknown. Here we report that maintenance of endothelial barrier integrity during leukocyte diapedesis requires local endothelial RhoA cycling. Endothelial RhoA depletion in vitro or Rho inhibition in vivo provokes neutrophil-induced vascular leakage that manifests during the physical movement of neutrophils through the endothelial layer. Local RhoA activation initiates the formation of contractile F-actin structures that surround emigrating neutrophils. These structures that surround neutrophil-induced endothelial pores prevent plasma leakage through actomyosin-based pore confinement. Mechanistically, we found that the initiation of RhoA activity involves ICAM-1 and the Rho GEFs Ect2 and LARG. In addition, regulation of actomyosin-based endothelial pore confinement involves ROCK2b, but not ROCK1. Thus, endothelial cells assemble RhoA-controlled contractile F-actin structures around endothelial pores that prevent vascular leakage during leukocyte extravasation.
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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.