Evidence map›Paper›PMID 34278471›Full record

ArticleInternational journal of molecular medicine2021

miR‑29a‑3p regulates the epithelial‑mesenchymal transition via the SPARC/ERK signaling pathway in human bronchial epithelial cells.

Xiaobo Zhang, Jun Xie, Hongmei Sun, Qin Wei, Guangmin Nong

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Xiaobo ZhangPediatric Department, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China.
Jun XiePediatric Department, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China.
Hongmei SunPediatric Department, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China.
Qin WeiPediatric Department, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China.
Guangmin NongPediatric Department, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region 530021, P.R. China.
Guangxi Medical University · CNFirst Affiliated Hospital of GuangXi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophilic asthma (NA) is a subtype of asthma that responds poorly to corticosteroid treatment. In certain diseases, microRNA (miR)‑29a‑3p is considered to be a key regulatory molecule for remodeling of the extracellular matrix. However, the effect of miR‑29a‑3p on airway remodeling is unknown. The present study aimed to investigate the role of miR‑29a‑3p in NA. A mouse model of NA was established and these animals were compared to normal controls. Both groups of mice were subjected to lung function tests and histopathological analysis. Human bronchial epithelial cells (16HBE) were grown in culture and incubated with secreted protein acidic rich in cysteine (SPARC) and a miR‑29a‑3p mimic. The expression of miR‑29a‑3p, SPARC and epithelial‑mesenchymal transition (EMT)‑related markers were measured using reverse transcription‑quantitative PCR and western blotting. Luciferase reporter assay was performed to identify the direct regulatory relationship between miR‑29a‑3p and SPARC. miR‑29a‑3p expression was significantly decreased, while SPARC expression was increased in the NA mouse model with a phenotype of EMT. Overexpression of SPARC downregulated the expression of E‑cadherin, while it increased the expression of vimentin in 16HBE cells. miR‑29a‑3p administration reversed the SPARC‑induced effects on E‑cadherin and vimentin expression. Luciferase assays confirmed that SPARC was the target gene for miR‑29a‑3p. Furthermore, SPARC overexpression increased the protein expression of phosphorylated (p)‑ERK, while transfection with miR‑29a‑3p mimics significantly inhibited this increase. The data suggested that EMT in the NA mouse model was associated with decreased levels of miR‑29a‑3p and elevated SPARC. Furthermore, SPARC could induce the formation of EMT in 16HBE cells in vitro and this was directly targeted by miR‑29a‑3p and mediated by p‑ERK, suggesting that miR‑29a‑3p may participate in the airway remodeling of NA.

Indexed as

Epithelial-Mesenchymal TransitionMAP Kinase Signaling SystemAnimalsAsthmaBronchiCell LineEpithelial CellsFemaleGene Expression RegulationHumansMiceMice, Inbred C57BLMicroRNAsOsteonectinRespiratory MucosaSignal TransductionMicroRNAsMIRN29a microRNA, humanOsteonectinSPARC protein, humanbronchial epithelial cellepithelial‑mesenchymal transitionmicroRNA‑29a‑3pneutrophilic asthmasecreted protein acidic rich in cysteine

Identifiers

PMID34278471
PMCPMC8285050
OpenAlexW3183097292

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.