Evidence map›Paper›PMID 33760118›Full record

ArticleInternational journal of molecular medicine2021

Knockdown of long non‑coding RNA DLEU2 suppresses idiopathic pulmonary fibrosis by regulating the microRNA‑369‑3p/TRIM2 axis.

Hengzhong Yi, Danlin Luo, Yangbao Xiao, Di Jiang

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Development of a peripheral blood transcriptomic gene signature to predict bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2023
    Trial
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  13. Crosstalk of ubiquitin system and non-coding RNA in fibrosis.International journal of biological sciences · 2024
    Review
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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

4 authors at 2 institutions in 1 country.

Hengzhong YiSixth Medical Department, Hunan Chest Hospital, Changsha, Hunan 410013, P.R. China.
Danlin LuoSixth Medical Department, Hunan Chest Hospital, Changsha, Hunan 410013, P.R. China.
Yangbao XiaoEndoscopy Center, Hunan Chest Hospital, Changsha, Hunan 410013, P.R. China.
Di JiangDepartment of Ultrasound, The First Affiliated Hospital of University of South China, Hengyang, Hunan 421001, P.R. China.
Hunan Province Chest Hospital · CNFirst Affiliated Hospital of University of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is the most common form of idiopathic interstitial pneumonia with an increasing incidence. In the present study, Genome Expression Omnibus (GEO) datasets (GSE10667, GSE24206 and GSE32537) were applied to identify lncRNA DLEU2 in IPF. Through prediction using starBase, TargetScan, miRTarBase and miRDB, tripartite motif containing 2 (TRIM2) and prostaglandin F2 receptor inhibitor (PTGFRN) were found to be upregulated in IPF. DLEU2 expression, the mRNA expression of TRIM2 and PTGFRN, and miR‑369‑3p expression in A549 cells and lung tissues were detected by RT‑qPCR. The protein expression of TRIM2 and PTGFRN in lung tissues and A549 cells was detected by western blot analysis. The proliferation and migration of A549 cells was respectively detected by CCK‑8 assay and wound healing assay. The expression of collagen I, α‑smooth muscle actin (SMA) and E‑cadherin was detected by immunofluorescence assay in A549 cells, and collagen I expression was detected by immunohistochemistry assay in lung tissues. The expression of collagen I, α‑SMA and E‑cadherin was also detected by western blot analysis in A549 cells and lung tissues. Dual‑luciferase reporter assay was used to confirm the association between DLEU2 and miR‑369‑3p, and miR‑369‑3p and TRIM2. As a result, DLEU2 expression was found to be upregulated in IPF and in transforming growth factor (TGF)‑β1‑stimulated A549 cells. The silencing of DLEU2 inhibited the TGF‑β1‑induced proliferation, migration and epithelial‑mesenchymal transition (EMT) of A549 cells and bleomycin (BLM)‑induced pulmonary fibrosis in mice. TRIM2 expression was increased and miR‑369‑3p expression was decreased in the lung tissues of mice with BLM‑induced fibrosis and in TGF‑β1‑stimulated A549 cells. DLEU2 directly targeted miR‑369‑3p. The effect of the silencing of DLEU2 on TGF‑β1‑stimulated A549 cells was suppressed by the silencing of miR‑369‑3p. TRIM2 was the target protein of miR‑369‑3p. On the whole, the present study demonstrates that the silencing of DLEU2 suppressed IPF by upregulating miR‑369‑3p expression and downregulating TRIM2 expression.

Indexed as

A549 CellsAnimalsBleomycinCell MovementCell ProliferationDisease Models, AnimalEpithelial-Mesenchymal TransitionGene Expression RegulationHeterograftsHumansIdiopathic Pulmonary FibrosisMaleMiceMice, Inbred C57BLMicroRNAsRNA, Long NoncodingBleomycinDLEU2 lncRNA, humanMicroRNAsMIRN369 microRNA, humanRNA, Long NoncodingTransforming Growth Factor beta1TRIM2 protein, humanTripartite Motif ProteinsUbiquitin-Protein Ligasesidiopathic pulmonary fibrosislncRNA DLEU2miR‑369‑3ptripartite motif containing 2

Identifiers

PMID33760118
PMCPMC7979258
OpenAlexW3133664225

What Socratic 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 Socratic graph.