Evidence map›Paper›PMID 32852789›Full record

ArticleImmunology2021

MicroRNA-7 negatively regulates Toll-like receptor 4 signaling pathway through FAM177A.

Huizi Chen, Mengmeng Guo, Dongxu Yue, Juanjuan Zhao, Ya Zhou, Chao Chen, Guiyou Liang, Lin Xu

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 25% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Loss of function of FAM177A1, a Golgi complex localized protein, causes a novel neurodevelopmental disorder.Genetics in medicine : official journal of the American College of Medical Genetics · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. TCR repertoire landscape reveals macrophage-mediated clone deletion in endotoxin tolerance.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. MiR-7 in Cancer Development.Biomedicines · 2021
    Review
  19. 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

8 authors at 2 institutions in 1 country.

Huizi ChenSpecial Key Laboratory of Gene Detection & Therapy of Guizhou Province, Zunyi, China.ORCID 0000-0002-8914-8428
Mengmeng GuoSpecial Key Laboratory of Gene Detection & Therapy of Guizhou Province, Zunyi, China.
Dongxu YueSpecial Key Laboratory of Gene Detection & Therapy of Guizhou Province, Zunyi, China.
Juanjuan ZhaoSpecial Key Laboratory of Gene Detection & Therapy of Guizhou Province, Zunyi, China.
Ya ZhouDepartment of Medical Physics, Zunyi Medical University, Zunyi, China.
Chao ChenSpecial Key Laboratory of Gene Detection & Therapy of Guizhou Province, Zunyi, China.
Guiyou LiangDepartment of Cardiovascular Surgery, Affiliated Hospital of Guizhou Medical University, Guiyang, China.
Lin XuSpecial Key Laboratory of Gene Detection & Therapy of Guizhou Province, Zunyi, China.ORCID 0000-0002-6889-0279
Zunyi Medical University · CNGuiyang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptor (TLR) 4 signalling is critical for innate immunoinflammatory response and widely triggers the development of various types of clinical diseases. MicroRNA-7 (miR-7) is well documented to play an important regulatory role in various biological events. However, the exact role of miR-7 in TLR4 signalling pathway remains to be fully elucidated. In the present study, we found that miR-7 expression in TLR4 signalling-activated bone marrow-derived macrophages (BMDMs) stimulated by LPS was dramatically increased. Importantly, miR-7 deficiency significantly enhanced the production of related inflammatory cytokines including IL-1β, IL-6 and IL-12, as well as TNF-α, on LPS-activated BMDMs, accompanied by elevated transduction of TLR4 signalling including Myd88-dependent and Myd88-independent pathways, whereas miR-7 overexpression significantly decreased the transduction of TLR4 signalling and the production of related inflammatory cytokines. Mechanistically, we identified family with sequence similarity 177, member A (FAM177A) as a novel target molecule of miR-7. Furthermore, down-regulation of FAM177A using RNAi could impair the transduction of TLR4 signalling. Finally, down-regulation of FAM177A also reversed the effect of miR-7 deficiency on TLR4 signalling transduction and production of related inflammatory cytokines on BMDMs. Therefore, we provide the new evidence that miR-7 acts as a novel negative fine-tuner in regulating TLR4 signalling pathways by targeting FAM177A, which might throw light on the basal understanding on the regulatory mechanism of TLR4 signalling and benefit the development of therapeutic strategies against related clinical diseases.

Indexed as

AnimalsCell LineCytokinesDown-RegulationHEK293 CellsHumansInflammationMacrophagesMiceMice, Inbred C57BLMicroRNAsMyeloid Differentiation Factor 88RAW 264.7 CellsSignal TransductionToll-Like Receptor 4CytokinesMicroRNAsMIRN7-1 microRNA, humanMyeloid Differentiation Factor 88TLR4 protein, humanToll-Like Receptor 4FAM177ALPSmacrophagesmicroRNA-7TLR4

Identifiers

PMID32852789
PMCPMC7730018
OpenAlexW3080277513

What OpenQuestion holds

Textmetadata
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.