Evidence map›Paper›PMID 36275894›Full record

ArticleOxidative medicine and cellular longevity2022

Transcription Factor p300 Regulated miR-451b Weakens the Cigarette Smoke Extract-Induced Cellular Stress by Targeting RhoA/ROCK2 Signaling.

Wen Shen, Shukun Wang, Ruili Wang, Yang Zhang, Hong Tian, Xi Wang, Xin Wu, Xiaolei Yang, Wei Wei

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 42% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. 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.

Wen ShenDepartment of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, China.ORCID https://orcid.org/0000-0002-9973-2281
Shukun WangDepartment of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, China.ORCID https://orcid.org/0000-0003-3806-3181
Ruili WangDepartment of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, China.ORCID https://orcid.org/0000-0001-7164-2332
Yang ZhangDepartment of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, China.ORCID https://orcid.org/0000-0002-2487-8913
Hong TianDepartment of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, China.ORCID https://orcid.org/0000-0002-7887-0976
Xi WangDepartment of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, China.ORCID https://orcid.org/0000-0002-5954-0445
Xin WuDepartment of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, China.ORCID https://orcid.org/0000-0002-0537-9561
Xiaolei YangDepartment of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, China.ORCID https://orcid.org/0000-0002-5780-4697
Wei WeiDepartment of Respiratory Medicine, The Second Affiliated Hospital of Kunming Medical University, Kunming, China.ORCID https://orcid.org/0000-0001-8236-8017
Kunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: A previous study identified miR-451b as a potential biomarker in smoker with or without chronic obstructive pulmonary disease (COPD). However, the function and molecular mechanisms of miR-451b in the pathogenesis of COPD remain elusive. Methods: Macrophages and lung fibroblasts were exposed to 10% cigarette smoke extract (CSE) solution for 24 h. Expression miR-451b and its potential transcription factor p300 were detected. The association between p300 and miR-451b, miR-451b and RhoA was validated by luciferase reporter assay. The release of IL-12 and TNF- Results: Results showed that p300 and miR-451b was downregulated, while RhoA was upregulated in CSE-induced macrophages and lung fibroblasts. The stimulation of CSE promoted the degradation of p300 by ubiquitination, and RhoA was confirmed as the target gene of miR-451b. MiR-451b overexpression significantly decreased the release of IL-12 and TNF- Conclusions: Our data suggest that p300/miR-451b protects against CSE-induced cell stress possibly through downregulating RhoA/ROCK2 pathway.

Indexed as

Cigarette SmokingMicroRNAsPulmonary Disease, Chronic ObstructiveBiomarkersHumansInterleukin-12NicotianarhoA GTP-Binding Proteinrho-Associated KinasesTranscription FactorsTumor Necrosis Factor-alphaBiomarkersInterleukin-12MicroRNAsrhoA GTP-Binding ProteinRHOA protein, humanrho-Associated KinasesROCK2 protein, humanTranscription FactorsTumor Necrosis Factor-alpha

Identifiers

PMID36275894
PMCPMC9586727
OpenAlexW4306248937

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.