ArticleThe Journal of physiology1990
Role of actin and myosin in the control of paracellular permeability in pig, rat and human vascular endothelium.
Article in The Journal of physiology, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 198 citations in OpenAlex.
- A specific role for endothelial EPLIN-isoform-regulated actin dynamics in neutrophil transmigration.Scientific reports · 2025Article
- TNF-α induces VE-cadherin-dependent gap/JAIL cycling through an intermediate state essential for neutrophil transmigration.Frontiers in immunology · 2025Article
- Hypergravity Activates a Pro-Angiogenic Homeostatic Response by Human Capillary Endothelial Cells.International journal of molecular sciences · 2020Article
- Endothelial heterogeneity across distinct vascular beds during homeostasis and inflammation.eLife · 2020Article
- ZIPK mediates endothelial cell contraction through myosin light chain phosphorylation and is required for ischemic-reperfusion injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- A Novel Microscopic Assay Reveals Heterogeneous Regulation of Local Endothelial Barrier Function.Biophysical journal · 2019Article
- Role of PI3K/Akt and MEK/ERK Signalling in cAMP/Epac-Mediated Endothelial Barrier Stabilisation.Frontiers in physiology · 2019Article
- Polarized actin and VE-cadherin dynamics regulate junctional remodelling and cell migration during sprouting angiogenesis.Nature communications · 2017Article
- A CDC42-centered signaling unit is a dominant positive regulator of endothelial integrity.Scientific reports · 2017Article
- Contraction of endothelial cells: 40 years of research, but the debate still lives.Histochemistry and cell biology · 2016Review
- Interaction between Flavivirus and Cytoskeleton during Virus Replication.BioMed research international · 2015Review
- cAMP controls the restoration of endothelial barrier function after thrombin-induced hyperpermeability via Rac1 activation.Physiological reports · 2014Article
- Dynamics between actin and the VE-cadherin/catenin complex: novel aspects of the ARP2/3 complex in regulation of endothelial junctions.Cell adhesion & migration · 2014Review
- Myosin light chain kinase signaling in endothelial barrier dysfunction.Medicinal research reviews · 2013Review
- Role of NF-κB activation in LPS-induced endothelial barrier breakdown.Histochemistry and cell biology · 2012Article
- Recombinant human angiopoietin-1 ameliorates the expressions of ZO-1, occludin, VE-cadherin, and PKCα signaling after focal cerebral ischemia/reperfusion in rats.Journal of molecular neuroscience : MN · 2012Article
- Intermedin (adrenomedullin2) stabilizes the endothelial barrier and antagonizes thrombin-induced barrier failure in endothelial cell monolayers.British journal of pharmacology · 2012Article
- A new Ebola virus nonstructural glycoprotein expressed through RNA editing.Journal of virology · 2011Article
- Ultrastructural analysis reveals cAMP-dependent enhancement of microvascular endothelial barrier functions via Rac1-mediated reorganization of intercellular junctions.The American journal of pathology · 2011Article
- Myosin light chain kinase in microvascular endothelial barrier function.Cardiovascular research · 2010Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. We have investigated the endothelial actomyosin system with particular emphasis on its possible role in actively opening a paracellular route for permeability. 2. Actin and myosin comprised 16% of total endothelial protein with a molar actin/myosin ratio of 16.2 which is close to the actin/myosin ratio of muscle (studies on freshly isolated pig pulmonary arterial endothelial cells, PAEC). 3. By immunocytochemistry at the light and electron microscope levels the bulk of actin and myosin was colocalized in close vicinity to the intercellular clefts of both micro- and macrovascular endothelial cells in situ and in vitro. 4. Calcium-ionophore-induced rise in permeability of human umbilical venous endothelial cells (HUVEC) and PAEC monolayers grown on filters in a two-chamber permeability system was caused by opening of intercellular gaps. Gap formation depended on the rise in intracellular Ca2+ and could be blocked by the calmodulin-binding drugs trifluperazine (TFP) and W7. 5. In skinned monolayers of cultured PAEC and in isolated sheets of HUVEC gap formation was shown to require ATP and occurred only when free myosin binding sites were available on endothelial actin filaments (experiments with myosin subfragment 1 modified by N-ethylmaleimide, S1-NEM). 6. These experiments suggest that actin and myosin in endothelial cells play a central role in regulating the width of the intercellular clefts, thereby controlling the paracellular pathway of vascular permeability.
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