Evidence map›Paper›PMID 32583575›Full record

ArticleThe Kaohsiung journal of medical sciences2020

MiRNA-620 promotes TGF-β1-induced proliferation of airway smooth muscle cell through controlling PTEN/AKT signaling pathway.

Hui Chen, Su-Xiang Guo, Sai Zhang, Xiao-Dan Li, Hao Wang, Xiao-Wei Li

Open access · goldAbstract read
In one paragraph

Article in The Kaohsiung journal of medical sciences, 2020. 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
3.1field-weighted citation impact, top 8% 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. Article
  2. Article
  3. Noncoding RNAs in asthmatic airway smooth muscle cells.European respiratory review : an official journal of the European Respiratory Society · 2023
    Review
  4. Recent miRNA Research in Asthma.Current allergy and asthma reports · 2022
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  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

6 authors at 1 institution in 1 country.

Hui ChenDepartment of Pediatrics, Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin City, China.
Su-Xiang GuoDepartment of Pediatrics, Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin City, China.
Sai ZhangDepartment of Pediatrics, Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin City, China.ORCID https://orcid.org/0000-0002-4128-4797
Xiao-Dan LiDepartment of Pediatrics, Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin City, China.
Hao WangDepartment of Pediatrics, Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin City, China.
Xiao-Wei LiDepartment of Pediatrics, Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin City, China.
Tianjin University of Traditional Chinese Medicine · CN

Funding

National Natural Science Foundation of China (NSFC) 81904250
6 · The paper itself

Abstract

Asthma is an inflammatory syndrome characterized by airway hyperresponsiveness, bronchial inflammation, and airway remodeling. The hypertrophy and hyperplasia of airway smooth muscle cells (ASMCs) are hallmarks of bronchial remodeling in asthma. In this study, the regulatory effects of microRNA-620 (miR-620) on ASMC proliferation and apoptosis in response to transforming growth factor β1 (TGF-β1) stimulation was investigated. The expression of miR-620 was significantly upregulated in TGF-β1-treated ASMCs compared with vehicle-treated cells. Downregulation of miR-620 suppressed the proliferation and increased apoptosis in TGF-β1-stimulated ASMCs. Phosphatase and tensin homolog (PTEN) was predicted and confirmed as a downstream target of miR-620. PTEN was upregulated in miR-620-inhibitor transfected ASMCs, but decreased in cells delivered with miR-620 mimics. Moreover, knocking down miR-620 alone efficiently reduced the phosphorylation of protein kinase B (AKT), decreased TGF-β1-induced proliferation and promoted apoptosis in ASMCs, whereas downregulation of PTEN in miR-620 inhibitor-transfected cells restored the activation of AKT, increased TGF-β1-triggered proliferation, and partially inhibited ASMC apoptosis. Taken together, the present study provided evidence that miR-620 increased TGF-β1-mediated proliferation and suppressed apoptosis in ASMCs via the regulation of PTEN and AKT expression. These findings suggest that miR-620/PTEN/AKT axis may be considered as a therapeutic target for asthma treatment.

Indexed as

AntagomirsApoptosisBase PairingBase SequenceBronchiCell ProliferationGene Expression RegulationHumansMicroRNAsMyocytes, Smooth MuscleOligoribonucleotidesPrimary Cell CultureProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePteridinesSignal TransductionAntagomirsMicroRNAsMIRN620 microRNA, humanOligoribonucleotidesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanPteridinesSD-208TGFB1 protein, humanTransforming Growth Factor beta1airway smooth muscle cell (ASMC)microRNA-620 (miR-620)phosphatase and tensin homolog (PTEN)protein kinase B (AKT)transforming growth factor-β1 (TGF-β1)

Identifiers

PMID32583575
PMCPMC11896339
OpenAlexW3037487642

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.