Evidence map›Paper›PMID 31023490›Full record

ArticleImmunobiology2019

P53 supports endothelial barrier function via APE1/Ref1 suppression.

Mohammad A Uddin, Mohammad S Akhter, Agnieszka Siejka, John D Catravas, Nektarios Barabutis

Open access · bronzeAbstract read
In one paragraph

Article in Immunobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Growth hormone - releasing hormone in the immune system.Reviews in endocrine & metabolic disorders · 2025
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  6. Article
  7. Article
  8. Review
  9. Article
  10. Unfolded protein response in endothelial injury.Cell cycle (Georgetown, Tex.) · 2022
    Article
  11. Article
  12. Tunicamycin Protects against LPS-Induced Lung Injury.Pharmaceuticals (Basel, Switzerland) · 2022
    Article
  13. Article
  14. Vitexin inhibits APEX1 to counteract the flow-induced endothelial inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. P53 deficiency potentiates LPS-Induced acute lung injuryCurrent research in physiology · 2020
    Article
  20. P53 in the impaired lungs.DNA repair · 2020
    Review
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

5 authors at 3 institutions in 2 countries.

Mohammad A UddinSchool of Basic Pharmaceutical and Toxicological Sciences, College of Pharmacy, University of Louisiana Monroe, Monroe, LA, 71201, USA.
Mohammad S AkhterSchool of Basic Pharmaceutical and Toxicological Sciences, College of Pharmacy, University of Louisiana Monroe, Monroe, LA, 71201, USA.
Agnieszka SiejkaDepartment of Clinical Endocrinology, Medical University of Lodz, Poland.
John D CatravasSchool of Medical Diagnostic and Translational Sciences, College of Health Sciences, Old Dominion University, Norfolk, VA, USA; Departments of Medicine and Physiological Sciences, Eastern Virginia Medical School, Norfolk, VA, USA.
Nektarios BarabutisSchool of Basic Pharmaceutical and Toxicological Sciences, College of Pharmacy, University of Louisiana Monroe, Monroe, LA, 71201, USA. Electronic address: barabutis@ulm.edu.
University of Louisiana at Monroe · USMedical University of Lodz · PLOld Dominion University · US

Funding

STABILITY' (symptomatic review during biologic therapy) Review in Inflammatory Bowel DiseaseP20GM103424 · NIGMS · LOUISIANA STATE UNIV A&M COL BATON ROUGE · PI Seetharama D Jois · 2012 to 2026
$57.4M
NIGMS NIH HHS P20 GM103424
6 · The paper itself

Abstract

The tumor suppressor protein P53 is strongly involved in orchestrating cellular defenses in the diverse variety of human tissues. Anomalies to lung endothelium permeability are streaming severe consequences towards human health, often associated with fatal outcomes. Ongoing investigations suggest that P53 exerts a prominent strategic role in crucial signaling cascades, in charge of both the maintenance and defense of pulmonary endothelium against toxic intruders. The current study employs human and bovine lung microvascular cells, as well as pharmacologic and genetic P53 modulators to demonstrate the negative regulation of APE1/Ref1 by P53. Moreover, it includes real time measurements of endothelial permeability, to reveal the disruptive role of APE1/Ref1 towards endothelial integrity. Those findings supports our efforts to elucidate the highly sophisticated regulatory network that enact endothelial adaptations under the plethora of challenging environmental factors.

Indexed as

Capillary PermeabilityCells, CulturedDisease SusceptibilityDNA-(Apurinic or Apyrimidinic Site) LyaseEndothelial CellsEndothelium, VascularGene Expression RegulationGene SilencingHSP90 Heat-Shock ProteinsHumansRNA InterferenceTumor Suppressor Protein p53APEX1 protein, humanDNA-(Apurinic or Apyrimidinic Site) LyaseHSP90 Heat-Shock ProteinsTumor Suppressor Protein p53Acute Lung InjuryAcute Respiratory Distress SyndromeHsp90 inhibitorsInflammation

Identifiers

PMID31023490
PMCPMC6682453
OpenAlexW2937773805

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.