ArticleAmerican journal of physiology. Cell physiology2012
p120-Catenin prevents neutrophil transmigration independently of RhoA inhibition by impairing Src dependent VE-cadherin phosphorylation.
Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 34 citations in OpenAlex.
- Dialogue between VE-Cadherin and Sphingosine 1 Phosphate Receptor1 (S1PR1) for Protecting Endothelial Functions.International journal of molecular sciences · 2023Review
- Article
- GSTpi regulates VE-cadherin stabilization through promoting S-glutathionylation of Src.Redox biology · 2020Article
- The vascular endothelial specific IL-4 receptor alpha-ABL1 kinase signaling axis regulates the severity of IgE-mediated anaphylactic reactions.The Journal of allergy and clinical immunology · 2018Article
- Cortical Actin Dynamics in Endothelial Permeability.Current topics in membranes · 2018Article
- Neutrophil FcγRIIA promotes IgG-mediated glomerular neutrophil capture via Abl/Src kinases.The Journal of clinical investigation · 2017Article
- Protein Interactions at Endothelial Junctions and Signaling Mechanisms Regulating Endothelial Permeability.Circulation research · 2017Review
- Regulation of endothelial barrier function by p120-catenin∙VE-cadherin interaction.Molecular biology of the cell · 2017Article
- Integration of endothelial protease-activated receptor-1 inflammatory signaling by ubiquitin.Current opinion in hematology · 2016Review
- Left Ventricular T-Cell Recruitment Contributes to the Pathogenesis of Heart Failure.Circulation. Heart failure · 2015Article
- Regulation of Endothelial Adherens Junctions by Tyrosine Phosphorylation.Mediators of inflammation · 2015Review
- Control of vascular permeability by adhesion molecules.Tissue barriers · 2015Article
- VE-cadherin-independent cancer cell incorporation into the vascular endothelium precedes transmigration.PloS one · 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
- Emerging understanding of roles for arterioles in inflammation.Microcirculation (New York, N.Y. : 1994) · 2013Review
- Novel role of CD47 in rat microvascular endothelium: signaling and regulation of T-cell transendothelial migration.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- Endothelial junction regulation: a prerequisite for leukocytes crossing the vessel wall.Journal of innate immunity · 2013Review
- Intercellular adhesion molecules (ICAMs) and spermatogenesis.Human reproduction updateReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Leukocyte transendothelial migration (TEM) is regulated by several signaling pathways including Src family kinases (SFK) and the small RhoGTPases. Previous studies have shown that vascular endothelial-cadherin (VE-cad) forms a complex with β-,γ-, and p120-catenins and this complex disassociates to form a transient gap during leukocyte TEM. Additionally, p120-catenin (p120-1A) overexpression in human umbilical vein endothelial cells (HUVEC) stabilizes VE-cad surface expression, prevents tyrosine phosphorylation of VE-cad, and inhibits leukocyte TEM. Based on reports showing that p120 overexpression in fibroblasts or epithelial cells inhibits RhoA and activates Rac and Cdc42 GTPases, and on other reports showing that RhoA activation in endothelial cells is necessary for leukocyte TEM, we reasoned that p120 overexpression inhibited TEM through inhibition of RhoA. To test this idea, we overexpressed a mutant p120 isoform, p120-4A, which does not interact with RhoA. p120-4A colocalized with VE-cad in HUVEC junctions and enhanced VE-cad surface expression, similar to overexpression of p120-1A. Interestingly, overexpression of either p120-4A or p120-1A dramatically blocked TEM, and overexpression of p120-1A in HUVEC did not affect RhoA basal activity or activation of RhoA and Rac induced by thrombin or ICAM-1 crosslinking. In contrast, biochemical studies revealed that overexpression of p120-1A reduced activated pY416-Src association with VE-cad. In summary, p120 overexpression inhibits neutrophil TEM independently of an effect on RhoA or Rac and instead blocks TEM by preventing VE-cad tyrosine phosphorylation and association of active Src with the VE-cad complex.
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.