Evidence map›Paper›PMID 27546996›Full record

ArticleMediators of inflammation2016

Pancreatic Acinar Cells Employ miRNAs as Mediators of Intercellular Communication to Participate in the Regulation of Pancreatitis-Associated Macrophage Activation.

Yong Zhao, Hao Wang, Ming Lu, Xin Qiao, Bei Sun, Weihui Zhang, Dongbo Xue

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  9. Review
  10. Extracellular vesicles and pancreatitis: mechanisms, status and perspectives.International journal of biological sciences · 2021
    Review
  11. Article
  12. Review
  13. Article
  14. Exosomes and pancreatic diseases: status, challenges, and hopes.International journal of biological sciences · 2019
    Review
  15. Article
  16. Article
  17. Review
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

7 authors at 2 institutions in 2 countries.

Yong ZhaoDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.
Hao WangDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.
Ming LuDepartment of Surgery, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90064, USA.ORCID 0000-0003-1574-9850
Xin QiaoDepartment of Surgery, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90064, USA.
Bei SunDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.
Weihui ZhangDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.ORCID 0000-0002-3180-3004
Dongbo XueDepartment of General Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.ORCID 0000-0002-2675-8472
Harbin Medical University · CNUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophage activation plays an important role in the inflammatory response in acute pancreatitis. In the present study, the activation of AR42J pancreatic acinar cells was induced by taurolithocholate treatment. The results showed that the culture medium from the activated AR42J cells significantly enhanced NFκB activation in the macrophages compared to that without taurolithocholate treatment. Additionally, the precipitates obtained from ultracentrifugation of the culture media that were rich in exosomes were markedly more potent in activating macrophages compared with the supernatant fraction lacking exosomes. The results indicated that the mediators carried by the exosomes played important roles in macrophage activation. Exosomal miRNAs were extracted and examined using microarrays. A total of 115 differentially expressed miRNAs were identified, and 30 showed upregulated expression, while 85 displayed downregulated expression. Target genes of the differentially expressed miRNAs were predicted using TargetScan, MiRanda, and PicTar software programs. The putative target genes were subjected to KEGG functional analysis. The functions of the target genes were primarily enriched in MAPK pathways. Specifically, the target genes regulated macrophage activation through the TRAF6-TAB2-TAK1-NIK/IKK-NFκB pathway. As the mediators of signal transduction, miRNAs and their predicted target mRNAs regulate every step in the MAPK pathway.

Indexed as

Acinar CellsAnimalsCell LineCell SurvivalElectrophoretic Mobility Shift AssayExosome Multienzyme Ribonuclease ComplexMacrophagesMicroRNAsNF-kappa BPancreasPancreatitisRatsReal-Time Polymerase Chain ReactionSignal TransductionTrypsinogenExosome Multienzyme Ribonuclease ComplexMicroRNAsNF-kappa BTrypsinogen

Identifiers

PMID27546996
PMCPMC4980583
OpenAlexW2476227258

What OpenQuestion holds

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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.