Evidence map›Paper›PMID 32757169›Full record

ArticleGenes & genomics2020

MiR-339 attenuates LPS-induced intestinal epithelial cells inflammatory responses and apoptosis by targeting TLR4.

Meiying Xie, Lina Zhang, Luoye Li, Minhuan Fan, Lianjie Hou

Abstract read
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In one paragraph

Article in Genes & genomics, 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
–field-weighted citation impact
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.

  1. Article
  2. Review
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  6. Article
  7. Repairing gut barrier by traditional Chinese medicine: roles of gut microbiota.Frontiers in cellular and infection microbiology · 2024
    Review
  8. Article
  9. Review
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  11. Article
  12. Review
  13. Article
  14. Nontoxic-dose deoxynivalenol aggravates lipopolysaccharides-induced inflammation and tight junction disorder in IPEC-J2 cells through activation of NF-κB and LC3B.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020
    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

5 authors.

Meiying XieCollaborative Innovation Center of Plant Pest Management and Bioenvironmental Health Application Technology, Guangdong Eco-Engineering Polytechnic, 297 Guangshan First Road, Tianhe District, Guangzhou, 510520, Guangdong, China.
Lina ZhangCollaborative Innovation Center of Plant Pest Management and Bioenvironmental Health Application Technology, Guangdong Eco-Engineering Polytechnic, 297 Guangshan First Road, Tianhe District, Guangzhou, 510520, Guangdong, China.
Luoye LiCollaborative Innovation Center of Plant Pest Management and Bioenvironmental Health Application Technology, Guangdong Eco-Engineering Polytechnic, 297 Guangshan First Road, Tianhe District, Guangzhou, 510520, Guangdong, China.
Minhuan FanCollaborative Innovation Center of Plant Pest Management and Bioenvironmental Health Application Technology, Guangdong Eco-Engineering Polytechnic, 297 Guangshan First Road, Tianhe District, Guangzhou, 510520, Guangdong, China.
Lianjie HouQingyuan City People's Hospital, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan, 511518, Guangdong, China. 993841758@scau.edu.cn.ORCID 0000-0001-8314-9756

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIntestinal epithelial cells are important for defending against pathogen infection. LPS is an endotoxin that is highly antigenic and cytotoxic produced by bacteria. LPS disrupts the intestine epithelium integrity and induced the intestinal epithelial cell inflammation and apoptosis. Our previous study has predicted the function of exosome miRNAs through bioinformatics analysis, and we found that miR-339 had a potential function in cell inflammation response. To our knowledge, no published paper has demonstrated the miR-339 function in protecting the intestine epithelium against bacterial infection.

objectiveThe objective of this study is to evaluate the miR-339 function in regulating intestinal epithelial cells to defend against bacterial infection through biological experiments and bioinformatics analyses.

methodsThrough the miR-339 transfection experiment and TLR4 interfering experiment, we evaluated the function of miR-339 and TLR4 in the process of inflammatory responses and apoptosis. Through Bioinformatics analyses and dual-luciferase reporter experiment, we identified the target gene of miR-339.

resultsmiR-339 attenuates LPS-induced intestinal epithelial cells inflammatory responses through the TLR4/NF-κB signaling pathway and inhibited LPS-induced apoptosis through the P53 signaling pathway. TLR4 is the target gene of miR-339. TLR4 reduced LPS-induced proinflammatory responses and apoptosis.

conclusionsIn conclusion, miR-339 protected the intestine epithelial cells from LPS-induced cell inflammation and apoptosis through targeting TLR4. This study expanded our understanding of how miRNAs and genes work collaboratively in regulating intestinal epithelial cells to defend against bacterial infection.

Indexed as

AnimalsApoptosisCell LineChinaDatabases, GeneticEpithelial CellsExosomesHumansInflammationIntestinal MucosaIntestinesLipopolysaccharidesMicroRNAsSignal TransductionSwineToll-Like Receptor 4LipopolysaccharidesMicroRNAsMIRN339 microRNA, humanToll-Like Receptor 4ApoptosisInflammatory responsesMiR-339NF-κBP53

Identifiers

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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.