Evidence map›Paper›PMID 20724706›Full record

ArticleCirculation research2010

Kruppel-like factor-4 transcriptionally regulates VE-cadherin expression and endothelial barrier function.

Colleen E Cowan, Erin E Kohler, Tracey A Dugan, M Kamran Mirza, Asrar B Malik, Kishore K Wary

Open access · bronzeAbstract read
In one paragraph

Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Endothelial to mesenchymal transition: a central mechanism in diabetes-induced vascular pathology.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Micro-Executor of Natural Products in Metabolic Diseases.Molecules (Basel, Switzerland) · 2023
    Review
  18. Article
  19. Review
  20. Review

20 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Colleen E CowanDepartment of Pharmacology, University of Illinois, 835 S Wolcott, Room E403, Mail code 868, Chicago, IL 60612, USA.
Erin E Kohler
Tracey A Dugan
M Kamran Mirza
Asrar B Malik
Kishore K Wary
University of Illinois Chicago · US

Funding

TRAINING PROGRAM IN LUNG BIOLOGY AND PATHOBIOLOGYT32HL007829 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DOLLY MEHTA · 1995 to 2026
$15.6M
CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR029879 · NCRR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MAZZONE, THEODORE · 2009 to 2011
$11.0M
Training in Mechanisms of Cardiovascular DiseasesT32HL072742 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI TOBACMAN, LARRY S · 2003 to 2013
$3.7M
Regulation of Wnt Signaling by PAP2b During AngiogenesisR01HL079356 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI WARY, KISHORE K · 2006 to 2016
$3.0M
Pharmacological Sciences Predoctoral Training ProgramT32GM070388 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MALIK, ASRAR B. · 2005 to 2009
$795k
NCRR NIH HHS UL1 RR029879NCRR NIH HHS UL1RR029879NHLBI NIH HHS HL079356-03S1NHLBI NIH HHS R01 HL079356NHLBI NIH HHS R01HL079356NHLBI NIH HHS T32 HL007829NHLBI NIH HHS T32HL007829NHLBI NIH HHS T32 HL072742NHLBI NIH HHS T32HL072742NIGMS NIH HHS T32 GM070388NIGMS NIH HHS T32GM070388
6 · The paper itself

Abstract

rationaleVascular endothelial (VE)-cadherin localized at adherens junctions (AJs) regulates endothelial barrier function. Because WNT (wingless) signaling-induced activation of the transcription factor Krüppel-like factor (KLF)4 may have an important role in mediating the expression of VE-cadherin and AJ integrity, we studied the function of KLF4 in regulating VE-cadherin expression and the control of endothelial barrier function.

objectiveThe goal of this study was to determine the transcriptional role of KLF4 in regulating VE-cadherin expression and endothelial barrier function. METHODS AND

resultsExpression analysis, microscopy, chromatin immunoprecipitation, electrophoretic mobility shift assays, and VE-cadherin-luciferase reporter experiments demonstrated that KLF4 interacted with specific domains of VE-cadherin promoter and regulated the expression of VE-cadherin at AJs. KLF4 knockdown disrupted the endothelial barrier, indicating that KLF4 is required for normal barrier function. In vivo studies in mice showed augmented lipopolysaccharide-induced lung injury and pulmonary edema following Klf4 depletion.

conclusionOur data show the key role of KLF4 in the regulation of VE-cadherin expression at the level of the AJs and in the acquisition of VE-cadherin-mediated endothelial barrier function. Thus, KLF4 maintains the integrity of AJs and prevents vascular leakage in response to inflammatory stimuli.

Indexed as

Adherens JunctionsAnimalsAntigens, CDCadherin 5CadherinsCapillary PermeabilityCells, CulturedEndothelial CellsGene Expression RegulationHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsLipopolysaccharidesMiceMice, KnockoutNeutrophilsAntigens, CDCadherin 5CadherinsKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsLipopolysaccharidesWnt3 ProteinWnt Proteins

Identifiers

PMID20724706
PMCPMC3018700
OpenAlexW2102717891

What OpenQuestion holds

Textmetadata
LicenceTDM
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.