Evidence map›Paper›PMID 26991692›Full record

ArticleJournal of cellular and molecular medicine2016

A20 deficiency leads to angiogenesis of pulmonary artery endothelial cells through stronger NF-κB activation under hypoxia.

Jing Li, Linlin Zhang, Yueming Zhang, Ying Liu, Hongyue Zhang, Liuping Wei, Tingting Shen, Chun Jiang, Daling Zhu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. NF-κB and pulmonary hypertension: Advances in mechanistic research and therapeutic applications.American heart journal plus : cardiology research and practice · 2025
    Review
  5. Protective role of zinc in the pathogenesis of respiratory diseases.European journal of clinical nutrition · 2023
    Review
  6. Article
  7. A20 Is Increased in Fetal Lung in a Sheep LPS Model of Chorioamnionitis.Oxidative medicine and cellular longevity · 2022
    Article
  8. Observational
  9. Article
  10. Article
  11. Endothelial microvesicles in hypoxic hypoxia diseases.Journal of cellular and molecular medicine · 2018
    Review
  12. 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

9 authors at 3 institutions in 2 countries.

Jing LiDepartment of Biopharmaceutical Sciences, Harbin Medical University, Daqing, Heilongjiang, China.
Linlin ZhangDepartment of Biopharmaceutical Sciences, Harbin Medical University, Daqing, Heilongjiang, China.
Yueming ZhangDepartment of Biopharmaceutical Sciences, Harbin Medical University, Daqing, Heilongjiang, China.
Ying LiuDepartment of Biopharmaceutical Sciences, Harbin Medical University, Daqing, Heilongjiang, China.
Hongyue ZhangDepartment of Biopharmaceutical Sciences, Harbin Medical University, Daqing, Heilongjiang, China.
Liuping WeiDepartment of Biopharmaceutical Sciences, Harbin Medical University, Daqing, Heilongjiang, China.
Tingting ShenDepartment of Biopharmaceutical Sciences, Harbin Medical University, Daqing, Heilongjiang, China.
Chun JiangDepartment of Biology, Georgia State University, Atlanta, GA, USA.
Daling ZhuDepartment of Biopharmaceutical Sciences, Harbin Medical University, Daqing, Heilongjiang, China.
Daqing City People's Hospital · CNHeilongjiang University · CNGeorgia State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A20 is a zinc finger protein associated with hypoxia. As chronic hypoxia is responsible for intimal hyperplasia and disordered angiogenesis of pulmonary artery, which are histological hallmarks of pulmonary artery hypertension, we intended to explore the role of A20 in angiogenesis of pulmonary artery endothelial cells (ECs). Here, we found a transient elevation of A20 expression in the lung tissues from hypoxic rats compared with normoxic controls. This rapid enhancement was mainly detected in the endothelium, and similar results were reproduced in vitro. During early hypoxia, genetic inhibition of A20 increased proliferation in pulmonary artery ECs, linking to advanced cell cycle progression as well as microtubule polymerization, and aggravated angiogenic effects including tube formation, cell migration and adhesion molecules expression. In addition, a negative feedback loop between nuclear factor-kappa B and A20 was confirmed. Our findings provide evidence for an adaptive role of A20 against pulmonary artery ECs angiogenesis via nuclear factor-kappa B activation.

Indexed as

Neovascularization, PhysiologicAnimalsCell Adhesion MoleculesCell CycleCell HypoxiaCell ProliferationDNA-Binding ProteinsEndothelial CellsFeedback, PhysiologicalMaleMicrotubulesModels, BiologicalNF-kappa BPulmonary ArteryRats, WistarRNA, MessengerCell Adhesion MoleculesDNA-Binding ProteinsNF-kappa BRNA, MessengerTNFAIP3 protein, ratTumor Necrosis Factor alpha-Induced Protein 3A20angiogenesishypoxianuclear factor-kappa Bpulmonary artery endothelial cells

Identifiers

PMID26991692
PMCPMC4929300
OpenAlexW2299431164

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.