Evidence map›Paper›PMID 32889801›Full record

ArticleAging2020

PTEN participates in airway remodeling of asthma by regulating CD38/Ca

Yuanyuan Wu, Yiyi Lu, Fan Zou, Xinping Fan, Xudong Li, Hongni Zhang, Haijuan Chen, Xiuzhen Sun, Yun Liu

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Observational
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Motoneuron-Specific PTEN Deletion in Mice Induces Neuronal Hypertrophy and Also Regeneration after Facial Nerve Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  11. Review
  12. Review
  13. Article
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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 1 institution in 1 country.

Yuanyuan WuDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi'an 710004, Shaanxi Province, PR China.
Yiyi LuDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi'an 710004, Shaanxi Province, PR China.
Fan ZouDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi'an 710004, Shaanxi Province, PR China.
Xinping FanDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi'an 710004, Shaanxi Province, PR China.
Xudong LiDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi'an 710004, Shaanxi Province, PR China.
Hongni ZhangDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi'an 710004, Shaanxi Province, PR China.
Haijuan ChenDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi'an 710004, Shaanxi Province, PR China.
Xiuzhen SunDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi'an 710004, Shaanxi Province, PR China.
Yun LiuDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi'an 710004, Shaanxi Province, PR China.
Second Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Both phosphatase and tensin homologue deleted on chromosome ten (PTEN) and cluster of differentiation 38 (CD38) have been suggested to be key regulators of the pathogenesis of asthma. However, the precise role and molecular mechanisms by which PTEN and CD38 are involved in airway remodeling throughout asthma pathogenesis remains poorly understood. This study aimed to elucidate the role of PTEN and CD38 in airway remodeling of asthma. Exposure to tumor necrosis factor-α (TNF-α) in airway smooth muscle (ASM) cells markedly decreased PTEN expression, and increased expression of CD38. Overexpression of PTEN suppressed the expression of CD38 and downregulated proliferation and migration induced by TNF-α stimulation, which was partially reversed by CD38 overexpression. PTEN/CD38 axis regulated Ca2+ levels and cyclic AMP response-element binding protein (CREB) phosphorylation in TNF-α-stimulated ASM cells. The in vitro knockdown of CD38 or overexpression of PTEN remarkably restricted airway remodeling and decreased Ca2+ concentrations and CREB phosphorylation in asthmatic mice. CD38 overexpression abolished the inhibitory effects of PTEN overexpression on airway remodeling. These findings demonstrate that PTEN inhibits airway remodeling of asthma through the downregulation of CD38-mediated Ca2+/CREB signaling, highlighting a key role of PTEN/CD38/Ca2+/CREB signaling in the molecular pathogenesis of asthma.

Indexed as

Airway RemodelingCalcium SignalingADP-ribosyl Cyclase 1AnimalsAsthmaCell MovementCell ProliferationCells, CulturedCyclic AMP Response Element-Binding ProteinDisease Models, AnimalFemaleGene Expression RegulationMembrane GlycoproteinsMice, Inbred BALB CMyocytes, Smooth MusclePhosphorylationADP-ribosyl Cyclase 1Cd38 protein, mouseCreb1 protein, mouseCyclic AMP Response Element-Binding ProteinMembrane GlycoproteinsPTEN PhosphohydrolasePten protein, mouseTumor Necrosis Factor-alphaairway remodelingasthmaCD38CREBPTEN

Identifiers

PMID32889801
PMCPMC7485701
OpenAlexW3080203002

What Socratic 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 Socratic graph.