Evidence map›Paper›PMID 32767729›Full record

ArticleJournal of cellular and molecular medicine2020

Negative feedback loop of ERK/CREB/miR-212-3p inhibits HBeAg-induced macrophage activation.

Wenjun Chen, Hongjun Bian, Xiaoyu Xie, Xia Yang, Benjun Bi, Chunliu Li, Yuejuan Zhang, Qiang Zhu, Jing Song, Chengyong Qin and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  8. Review
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  10. Virulence · 2022
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  13. Article
  14. Review
  15. Hepatitis B virus e antigen and viral persistence.Current opinion in virology · 2021
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

11 authors at 3 institutions in 1 country.

Wenjun ChenShandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Hongjun BianShandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Xiaoyu XieShandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Xia YangShandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Benjun BiThe Affiliated Hospital of Qingdao University, Qingdao, China.
Chunliu LiYantai Affiliated Hospital of Binzhou Medical University, Yantai, China.
Yuejuan ZhangThe Affiliated Hospital of Qingdao University, Qingdao, China.
Qiang ZhuShandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Jing SongThe Affiliated Weihai Second Municipal Hospital of Qingdao University, Weihai, China.
Chengyong QinShandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Jianni QiShandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.ORCID 0000-0002-9512-7762
Shandong University · CNQingdao University · CNBinzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The activation of liver macrophages is closely related to liver injury after HBV infection. Our previous results demonstrated that HBeAg played a key role in inducing macrophage activation. As we all know, miRNAs are involved in the regulation of multiple immune cell functions. Meanwhile, we have shown that miR-155 positively regulates HBeAg-induced macrophage activation and accelerates liver injury. Subsequently, based on our previous miRNA sequencing results, we further evaluated the role of miR-212-3p called 'neurimmiR' in HBeAg-induced macrophages in this study. First, miR-212-3p expression was significantly elevated in HBeAg-treated macrophages. Meanwhile, we found up-regulation of miR-212-3p significantly decreased the production of cytokines, whereas knockdown of miR-212-3p held the opposite effect by gains and losses of function. Mechanically, although MAPK signal pathway, including ERK, JNK and p38, was activated in HBeAg-induced macrophages, only ERK promoted the expression of miR-212-3p via transcription factor CREB, which was able to bind to the promoter of miR-212-3p verified by ChIP assay. Moreover, we further indicated that up-regulated miR-212-3p inhibited HBeAg-induced inflammatory cytokine production through targeting MAPK1. In conclusion, miR-212-3p was augmented in HBeAg-stimulated macrophages via ERK/CREB signal pathway and the elevated miR-212-3p suppressed inflammatory cytokine production induced by HBeAg through targeting MAPK1.

Indexed as

AnimalsChromatin ImmunoprecipitationCyclic AMP Response Element-Binding ProteinCytokinesFeedback, PhysiologicalGene Expression RegulationHepatitis B e AntigensHumansInflammationMacrophage ActivationMAP Kinase Signaling SystemMiceMicroRNAsMonocytesPromoter Regions, GeneticProtein BindingCREB1 protein, humanCyclic AMP Response Element-Binding ProteinCytokinesHepatitis B e AntigensMicroRNAsMIRN212 microRNA, humanCREBHBeAgmacrophageMAPK1miR-212-3p

Identifiers

PMID32767729
PMCPMC7521245
OpenAlexW3048018380

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.