Evidence map›Paper›PMID 31396656›Full record

ArticleCellular and molecular life sciences : CMLS2020

Compensatory increase of VE-cadherin expression through ETS1 regulates endothelial barrier function in response to TNFα.

Natalia Colás-Algora, Diego García-Weber, Cristina Cacho-Navas, Susana Barroso, Alvaro Caballero, Catalina Ribas, Isabel Correas, Jaime Millán

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

8 authors at 4 institutions in 2 countries.

Natalia Colás-AlgoraCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), 28049, Madrid, Spain.
Diego García-WeberCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), 28049, Madrid, Spain. diego.garcia@inserm.fr.
Cristina Cacho-NavasCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), 28049, Madrid, Spain.
Susana BarrosoCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), 28049, Madrid, Spain.
Alvaro CaballeroCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), 28049, Madrid, Spain.
Catalina RibasCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), 28049, Madrid, Spain.
Isabel CorreasCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), 28049, Madrid, Spain.
Jaime MillánCentro de Biología Molecular "Severo Ochoa" (CSIC-UAM), 28049, Madrid, Spain. jmillan@cbm.csic.es.ORCID http://orcid.org/0000-0003-3107-147X
Centro de Biología Molecular Severo Ochoa · ESCentro de Investigación en Red en Enfermedades Cardiovasculares · ESHospital Universitario de La Princesa · ESInserm · FR

Funding

NEUROBEHAVIORAL MECHANISMS OF DRUG ADDICTIONR01DA003817 · NIDA · ALBANY MEDICAL COLLEGE · PI GLICK, STANLEY D · 1985 to 2001
$370k
Consejería de Educación, Juventud y Deporte, Comunidad de Madrid B2017/BMD-3671-INFLAMUNEConsejería de Educación, Juventud y Deporte, Comunidad de Madrid S2017/BMD-3817 TomoXliverInstituto de Salud Carlos III PI18/01662Ministerio de Economía, Industria y Competitividad, Gobierno de España BFU2015-67266-RMinisterio de Economía, Industria y Competitividad, Gobierno de España SAF2017-88187-R
6 · The paper itself

Abstract

VE-cadherin plays a central role in controlling endothelial barrier function, which is transiently disrupted by proinflammatory cytokines such as tumor necrosis factor (TNFα). Here we show that human endothelial cells compensate VE-cadherin degradation in response to TNFα by inducing VE-cadherin de novo synthesis. This compensation increases adherens junction turnover but maintains surface VE-cadherin levels constant. NF-κB inhibition strongly reduced VE-cadherin expression and provoked endothelial barrier collapse. Bacterial lipopolysaccharide and TNFα upregulated the transcription factor ETS1, in vivo and in vitro, in an NF-κB dependent manner. ETS1 gene silencing specifically reduced VE-cadherin protein expression in response to TNFα and exacerbated TNFα-induced barrier disruption. We propose that TNFα induces not only the expression of genes involved in increasing permeability to small molecules and immune cells, but also a homeostatic transcriptional program in which NF-κB- and ETS1-regulated VE-cadherin expression prevents the irreversible damage of endothelial barriers.

Indexed as

Adherens JunctionsAnimalsAntigens, CDCadherin 5CadherinsCapillary PermeabilityEndothelial CellsGene SilencingHumansHuman Umbilical Vein Endothelial CellsInflammationMiceProteolysisProto-Oncogene Protein c-ets-1Tumor Necrosis Factor-alphaUp-RegulationAntigens, CDCadherin 5CadherinsETS1 protein, humanProto-Oncogene Protein c-ets-1Tumor Necrosis Factor-alphaAdherens junctionsDegradationEndothelial barrier functionETS1LPSNF-κBPermeabilityResolution of inflammationVE-cadherin

Identifiers

PMID31396656
PMCPMC11105044
OpenAlexW2967003118

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.