Evidence map›Paper›PMID 21444752›Full record

ArticleJournal of cell science2011

CRSBP-1/LYVE-1 ligands disrupt lymphatic intercellular adhesion by inducing tyrosine phosphorylation and internalization of VE-cadherin.

Wei-Hsien Hou, I-Hua Liu, Cheng C Tsai, Frank E Johnson, Shuan Shian Huang, Jung San Huang

Erratum issuedAbstract read
In one paragraph

Article in Journal of cell science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
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  5. Review
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  7. Review
  8. In Sickness and in Health: The Immunological Roles of the Lymphatic System.International journal of molecular sciences · 2021
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Lymphatic Regulation of Cellular Trafficking.Journal of clinical & cellular immunology · 2014
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Wei-Hsien HouDepartments of Biochemistry and Molecular Biology, St Louis University School of Medicine, Doisy Research Center, 1100 S. Grand Boulevard, St Louis, MO 63104, USA.
I-Hua Liu
Cheng C Tsai
Frank E Johnson
Shuan Shian Huang
Jung San Huang
Saint Louis University · USAuxagen (United States) · USExperimental Pathology Laboratories · US

Funding

Development of a Novel TGF-beta Antagonist for Treating Hepatic FibrosisRC1AA019233 · NIAAA · SAINT LOUIS UNIVERSITY · PI HUANG, JUNG S. · 2009 to 2010
$843k
Novel Antagonists for Ameliorating Pulmonary FibrosisR41HL087463 · NHLBI · AUXAGEN, INC. · PI HUANG, JUNG S. · 2007 to 2007
$199k
Novel Therapeutic Agents for Diabetic UlcersR41DK078438 · NIDDK · AUXAGEN, INC. · PI HUANG, JUNG S. · 2008 to 2008
$182k
NHLBI NIH HHS HL 087463-01NHLBI NIH HHS R41 HL087463NIAAA NIH HHS AA 019233NIAAA NIH HHS DK 078438/AA 019223NIAAA NIH HHS RC1 AA019233NIDDK NIH HHS R41 DK078438
6 · The paper itself

Abstract

Cell-surface retention sequence (CRS) binding protein (CRSBP-1) is a membrane glycoprotein identified by its ability to bind PDGF-BB and VEGF-A via their CRS motifs (clusters of basic amino acid residues). CRSBP-1 is identical to LYVE-1 and exhibits dual ligand (CRS-containing proteins and hyaluronic acid) binding activity, suggesting the importance of CRSBP-1 ligands in lymphatic function. Here, we show that CRSBP-1 ligands induce disruption of VE-cadherin-mediated intercellular adhesion and opening of intercellular junctions in lymphatic endothelial cell (LEC) monolayers as determined by immunofluorescence microscopy and Transwell permeability assay. This occurs by interaction with CRSBP-1 in the CRSBP-1-PDGFβR-β-catenin complex, resulting in tyrosine phosphorylation of the complex, dissociation of β-catenin and p120-catenin from VE-cadherin, and internalization of VE-cadherin. Pretreatment of LECs with a PDGFβR kinase inhibitor abolishes ligand-stimulated tyrosine phosphorylation of VE-cadherin, halts the ligand-induced disruption of VE-cadherin intercellular adhesion and blocks the ligand-induced opening of intercellular junctions. These CRSBP-1 ligands also induce opening of lymphatic intercellular junctions that respond to PDGFβR kinase inhibitor in wild-type mice (but not in Crsbp1-null mice) as evidenced by increased transit of injected FITC-dextran and induced edema fluid from the interstitial space into lymphatic vessels. These results disclose a novel mechanism involved in the opening of lymphatic intercellular junctions.

Indexed as

AnimalsAntigens, CDbeta CateninCadherin 5CadherinsCell AdhesionCell LineEndothelial CellsHyaluronic AcidLigandsMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutPhosphorylationProtein BindingAntigens, CDbeta CateninCadherin 5Cadherinscell-surface retention-binding protein 1Hyaluronic AcidLigandsMembrane ProteinsReceptor, Platelet-Derived Growth Factor betaTyrosine

Identifiers

PMID21444752
PMCPMC3065383
OpenAlexW1996878266

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.