Evidence map›Paper›PMID 26227240›Full record

ArticleScientific reports2015

miR-628, a microRNA that is induced by Toll-like receptor stimulation, regulates porcine innate immune responses.

He Jun, He Ying, Chen Daiwen, Yu Bing, Mao Xiangbing, Zheng Ping, Yu Jie, Huang Zhiqing, Luo Junqiu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. miR-628 Promotes Burn-Induced Skeletal Muscle Atrophy via Targeting IRS1.International journal of biological sciences · 2016
    Article
  8. 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

9 authors at 2 institutions in 1 country.

He Jun1] Institute of Animal Nutrition, Sichuan Agricultural University, Ya'an, Sichuan 625014, P. R. China [2] Key Laborotary of Animal Disease-Resistance Nutrition, Ministry of Education, China.
He Ying1] Institute of Animal Nutrition, Sichuan Agricultural University, Ya'an, Sichuan 625014, P. R. China [2] Key Laborotary of Animal Disease-Resistance Nutrition, Ministry of Education, China.
Chen Daiwen1] Institute of Animal Nutrition, Sichuan Agricultural University, Ya'an, Sichuan 625014, P. R. China [2] Key Laborotary of Animal Disease-Resistance Nutrition, Ministry of Education, China.
Yu Bing1] Institute of Animal Nutrition, Sichuan Agricultural University, Ya'an, Sichuan 625014, P. R. China [2] Key Laborotary of Animal Disease-Resistance Nutrition, Ministry of Education, China.
Mao Xiangbing1] Institute of Animal Nutrition, Sichuan Agricultural University, Ya'an, Sichuan 625014, P. R. China [2] Key Laborotary of Animal Disease-Resistance Nutrition, Ministry of Education, China.
Zheng Ping1] Institute of Animal Nutrition, Sichuan Agricultural University, Ya'an, Sichuan 625014, P. R. China [2] Key Laborotary of Animal Disease-Resistance Nutrition, Ministry of Education, China.
Yu Jie1] Institute of Animal Nutrition, Sichuan Agricultural University, Ya'an, Sichuan 625014, P. R. China [2] Key Laborotary of Animal Disease-Resistance Nutrition, Ministry of Education, China.
Huang Zhiqing1] Institute of Animal Nutrition, Sichuan Agricultural University, Ya'an, Sichuan 625014, P. R. China [2] Key Laborotary of Animal Disease-Resistance Nutrition, Ministry of Education, China.
Luo Junqiu1] Institute of Animal Nutrition, Sichuan Agricultural University, Ya'an, Sichuan 625014, P. R. China [2] Key Laborotary of Animal Disease-Resistance Nutrition, Ministry of Education, China.
Sichuan Agricultural University · CNMinistry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mammalian innate and acquired immune responses involve a coordinated, sequential, and self limiting sequence of events controlled by positive and negative regulatory mechanism. MicroRNAs have been implicated as a negative regulator for diverse biological events including immune responses. However, the involvement of miRNAs in regulating the immune responses is just beginning to be explored. Here, we characterized the expression profiling of 375 microRNAs in porcine monocytes induced by lipopolysaccharide (LPS), and result shows that several of them are endotoxin-responsive genes. Through promoter analysis, the miR-628 was found to be a NF-κB dependent gene. Importantly, miR-628 was predicted to base-pair with sequences in the 3'-UTR of the myeloid differentiation protein 88 (MyD88) gene. And we found that the UTR inhibit expression of a linked reporter gene coding a key adapter molecule downstream of Toll-like receptors (TLRs), resulting in suppressing of the TLR signaling. Therefore, we not only propose a role of miR-628 in control of the TLR signaling through a negative feedback regulation loop involving down-regulation of MyD88 protein levels, but results may also contribute to rational target selection orchestrating the inflammatory responses.

Indexed as

3' Untranslated RegionsAnimalsCells, CulturedGene Expression RegulationImmediate-Early ProteinsImmunity, InnateLipopolysaccharidesMicroRNAsMonocytesMyeloid Differentiation Factor 88NF-kappa BPromoter Regions, GeneticSignal TransductionSus scrofaToll-Like Receptors3' Untranslated RegionsImmediate-Early ProteinsLipopolysaccharidesMicroRNAsMyeloid Differentiation Factor 88NF-kappa BToll-Like Receptors

Identifiers

PMID26227240
PMCPMC4521185
OpenAlexW982864065

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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.