ReviewHistochemistry and cell biology2016
Contraction of endothelial cells: 40 years of research, but the debate still lives.
Review in Histochemistry and cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 26 citations in OpenAlex.
- VE-Cadherin-Actin Regulation Promotes Mechanotransduction and Monolayer Maturation Involving a Tension-Sensitive Intermediate State.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Molecular Mechanisms of Scombroid Food Poisoning.International journal of molecular sciences · 2023Review
- Tuning of Liver Sieve: The Interplay between Actin and Myosin Regulatory Light Chain Regulates Fenestration Size and Number in Murine Liver Sinusoidal Endothelial Cells.International journal of molecular sciences · 2022Article
- Molecular hydrogen is a potential protective agent in the management of acute lung injury.Molecular medicine (Cambridge, Mass.) · 2022Review
- Molecular hydrogen is a promising therapeutic agent for pulmonary disease.Journal of Zhejiang University. Science. B · 2022Article
- Enhanced endothelial barrier function by monoclonal antibody activation of vascular endothelial cadherin.American journal of physiology. Heart and circulatory physiology · 2021Article
- p90RSK-MAGI1 Module Controls Endothelial Permeability by Post-translational Modifications of MAGI1 and Hippo Pathway.Frontiers in cardiovascular medicine · 2020Article
- MicroRNA-126 Modulates Palmitate-Induced Migration in HUVECs by Downregulating Myosin Light Chain Kinase via the ERK/MAPK Pathway.Frontiers in bioengineering and biotechnology · 2020Article
- TIMAP inhibits endothelial myosin light chain phosphatase by competing with MYPT1 for the catalytic protein phosphatase 1 subunit PP1cβ.The Journal of biological chemistry · 2019Article
- Histamine causes endothelial barrier disruption via CaScientific reports · 2018Article
- Dynamic of VE-cadherin-mediated spermatid-Sertoli cell contacts in the mouse seminiferous epithelium.Histochemistry and cell biology · 2018Article
- Cortical Actin Dynamics in Endothelial Permeability.Current topics in membranes · 2018Article
- Actin dynamics in the regulation of endothelial barrier functions and neutrophil recruitment during endotoxemia and sepsis.Cellular and molecular life sciences : CMLS · 2017Review
- In focus in HCB: from cell biology to tissue structure and function.Histochemistry and cell biology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Force generation in non-muscle cells is vital for many cellular and tissue functions. Force-generating mechanisms include actomyosin-mediated contraction, actin polymerization that drives plasma membrane protrusions and filopodia as well as kinesin- and dynein-controlled transport of vesicles and organelles along the microtubule cytoskeleton. The actomyosin-mediated contractility and actin remodeling in both epithelium and endothelium were shown to have significant impact on cell migration, shape change and formation and control of intercellular junctions. In endothelium, contraction is supposed to control permeability for fluid and solutes. However, recent studies demonstrated the constitutive appearance of junction-associated intermittent lamellipodia (JAIL) that drive vascular endothelial cadherin (VE-cadherin) dynamics and control endothelial permeability. Since thrombin blocks JAIL formation and thus increases endothelial permeability, the concept of a simple Rho GTPase-controlled contraction, which is supposed to open endothelial junctions, becomes challenged. Furthermore, specific tyrosine phosphorylation sites of VE-cadherin and catenins have been shown to be involved in control of VE-cadherin-mediated cell adhesion. How the causal-mechanistic interdependency between contractility, VE-cadherin and catenin phosphorylation and JAIL-mediated dynamic remodeling of VE-cadherin is regulated is still an open question and needs to be further addressed.
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.