ArticleCellular signalling2016
Dual role of vinculin in barrier-disruptive and barrier-enhancing endothelial cell responses.
Article in Cellular signalling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- NCKAP1 coordinates focal adhesion and adherens junction dynamics in endothelial barrier maintenance and angiogenesis.iScience · 2026Article
- Article
- Vinculin Y822 phosphorylation regulates adhesion remodeling during cardiomyocyte maturation.Journal of cell science · 2025Article
- Article
- Gα12 and Gα13 proteins are required for transforming growth factor-β-induced myofibroblast differentiation.The Biochemical journal · 2024Article
- Anoctamin-1 is induced by TGF-β and contributes to lung myofibroblast differentiation.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Anoctamin-1 is induced by TGF-beta and contributes to lung myofibroblast differentiation.bioRxiv : the preprint server for biology · 2023Article
- Vinculin Identified as a Potential Biomarker in Hand-Arm Vibration Syndrome Based on iTRAQ and LC-MS/MS-Based Proteomic Analysis.Journal of proteome research · 2023Article
- Article
- Vinculin strengthens the endothelial barrier during vascular development.Vascular biology (Bristol, England) · 2023Article
- Review
- CRISPR-Based Activation of Endogenous Expression ofFrontiers in cell and developmental biology · 2021Article
- Oxidized Phospholipids in Control of Endothelial Barrier Function: Mechanisms and Implication in Lung Injury.Frontiers in endocrinology · 2021Review
- CX3CL1 Induces Vertebral Microvascular Barrier Dysfunction via the Src/P115-RhoGEF/ROCK Signaling Pathway.Frontiers in cellular neuroscience · 2020Article
- The mechanobiology of tight junctions.Biophysical reviews · 2019Review
- Time-Variant SRC Kinase Activation Determines Endothelial Permeability Response.Cell chemical biology · 2019Article
- Histamine causes endothelial barrier disruption via CaScientific reports · 2018Article
- Cholesterol crystals increase vascular permeability by inactivating SHP2 and disrupting adherens junctions.Free radical biology & medicine · 2018Article
- Autophagy inhibitor 3-methyladenine protects against endothelial cell barrier dysfunction in acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Vinculin is required to maintain glomerular barrier integrity.Kidney international · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Endothelial cell (EC) barrier disruption induced by edemagenic agonists such as thrombin is a result of increased actomyosin contraction and enforcement of focal adhesions (FA) anchoring contracting stress fibers, which leads to cell retraction and force-induced disruption of cell junctions. In turn, EC barrier enhancement by oxidized phospholipids (OxPAPC) and other agonists is a result of increased tethering forces due to enforcement of the peripheral actin rim and enhancement of cell-cell adherens junction (AJ) complexes promoting EC barrier integrity. This study tested participation of the mechanosensitive adaptor, vinculin, which couples FA and AJ to actin cytoskeleton, in control of the EC permeability response to barrier disruptive (thrombin) and barrier enhancing (OxPAPC) stimulation. OxPAPC and thrombin induced different patterns of FA remodeling. Knockdown of vinculin attenuated both, OxPAPC-induced decrease and thrombin-induced increase in EC permeability. Thrombin stimulated the vinculin association with FA protein talin and suppressed the interaction with AJ protein, VE-cadherin. In contrast, OxPAPC stimulated the vinculin association with VE-cadherin. Thrombin and OxPAPC induced different levels of myosin light chain (MLC) phosphorylation and caused different patterns of intracellular phospho-MLC distribution. Thrombin-induced talin-vinculin and OxPAPC-induced VE-cadherin-vinculin association were abolished by myosin inhibitor blebbistatin. Expression of the vinculin mutant unable to interact with actin attenuated EC permeability changes and MLC phosphorylation caused by both, thrombin and OxPAPC. These data suggest that the specific vinculin interaction with FA or AJ in different contexts of agonist stimulation is defined by development of regional actyomyosin-based tension and participates in both, the barrier-disruptive and barrier-enhancing endothelial responses.
Indexed as
Identifiers
What OpenQuestion holds
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.