ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Ezrin/radixin/moesin proteins differentially regulate endothelial hyperpermeability after thrombin.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 65 citations in OpenAlex.
- Curing the brain: in search for new astrocyte-specific therapies.Experimental & molecular medicine · 2026Review
- Evaluation of serum moesin and podocalyxin levels in patients with diabetes mellitus.Open medicine (Warsaw, Poland) · 2026Article
- Serum moesin is associated with cognitive impairment and glucose fluctuations in patients with type 2 diabetes.Diabetology & metabolic syndrome · 2025Article
- The Effect of Radixin on the Function and Expression of Organic Anion Transporting Polypeptide 1B1.Biology · 2025Article
- Metabolome-wide association identifies ferredoxin-1 (FDX1) as a determinant of cholesterol metabolism and cardiovascular risk in Asian populations.Nature cardiovascular research · 2025Article
- The role of chloride intracellular channel 4 in tumors.Cancer cell international · 2025Review
- Radixin: Roles in the Nervous System and Beyond.Biomedicines · 2024Review
- CLIC4 Regulates Endothelial Barrier Control by Mediating PAR1 Signaling via RhoA.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Serine/Threonine Protein Phosphatases 1 and 2A in Lung Endothelial Barrier Regulation.Biomedicines · 2023Review
- Profiling of plasma extracellular vesicles identifies proteins that strongly associate with patient's global assessment of disease activity in rheumatoid arthritis.Frontiers in medicine · 2023Article
- In vivo dissection of Rhoa function in vascular development using zebrafish.Angiogenesis · 2022Article
- An Actin-, Cortactin- and Ena-VASP-Linked Complex Contributes to Endothelial Cell Focal Adhesion and Vascular Barrier Regulation.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2022Article
- The ROCK-ezrin signaling pathway mediates LPS-induced cytokine production in pulmonary alveolar epithelial cells.Cell communication and signaling : CCS · 2022Article
- Piezo1 activation attenuates thrombin-induced blebbing in breast cancer cells.Journal of cell science · 2022Article
- Unlocking the Untapped Potential of Endothelial Kinase and Phosphatase Involvement in Sepsis for Drug Treatment Design.Frontiers in immunology · 2022Review
- Inflammatory Immune Cytokine TNF-α Modulates Ezrin Protein ActivationFrontiers in pharmacology · 2021Article
- Tumor necrosis factor-α requires Ezrin to regulate the cytoskeleton and cause pulmonary microvascular endothelial barrier damage.Microvascular research · 2021Article
- Cigarette Smoke and Nicotine-Containing Electronic-Cigarette Vapor Downregulate Lung WWOX Expression, Which Is Associated with Increased Severity of Murine Acute Respiratory Distress Syndrome.American journal of respiratory cell and molecular biology · 2021Article
- Moesin Is a Novel Biomarker of Endothelial Injury in Sepsis.Journal of immunology research · 2021Article
- Microbial tryptophan metabolites regulate gut barrier function via the aryl hydrocarbon receptor.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Endothelial cell (EC) barrier disruption induced by inflammatory agonists such as thrombin leads to potentially lethal physiological dysfunction such as alveolar flooding, hypoxemia, and pulmonary edema. Thrombin stimulates paracellular gap and F-actin stress fiber formation, triggers actomyosin contraction, and alters EC permeability through multiple mechanisms that include protein kinase C (PKC) activation. We previously have shown that the ezrin, radixin, and moesin (ERM) actin-binding proteins differentially participate in sphingosine-1 phosphate-induced EC barrier enhancement. Phosphorylation of a conserved threonine residue in the COOH-terminus of ERM proteins causes conformational changes in ERM to unmask binding sites and is considered a hallmark of ERM activation. In the present study we test the hypothesis that ERM proteins are phosphorylated on this critical threonine residue by thrombin-induced signaling events and explore the role of the ERM family in modulating thrombin-induced cytoskeletal rearrangement and EC barrier function. Thrombin promotes ERM phosphorylation at this threonine residue (ezrin Thr567, radixin Thr564, moesin Thr558) in a PKC-dependent fashion and induces translocation of phosphorylated ERM to the EC periphery. Thrombin-induced ERM threonine phosphorylation is likely synergistically mediated by protease-activated receptors PAR1 and PAR2. Using the siRNA approach, depletion of either moesin alone or of all three ERM proteins significantly attenuates thrombin-induced increase in EC barrier permeability (transendothelial electrical resistance), cytoskeletal rearrangements, paracellular gap formation, and accumulation of phospho-myosin light chain. In contrast, radixin depletion exerts opposing effects on these indexes. These data suggest that ERM proteins play important differential roles in the thrombin-induced modulation of EC permeability, with moesin promoting barrier dysfunction and radixin opposing it.
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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.