Evidence map›Paper›PMID 32780740›Full record

ArticlePloS one2020

Lack of TLR4 modifies the miRNAs profile and attenuates inflammatory signaling pathways.

Juan R Ureña-Peralta, Raúl Pérez-Moraga, Francisco García-García, Consuelo Guerri

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

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  6. Combination therapy of insulin-like growth factor I and BTP-2 markedly improves lipopolysaccharide-induced liver injury in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
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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

4 authors at 2 institutions in 1 country.

Juan R Ureña-PeraltaMolecular and cellular pathology of Alcohol Laboratory, Prince Felipe Research Center, Valencia, Spain.
Raúl Pérez-MoragaBioinformatics & Biostatistics Unit, Prince Felipe Research Center, Valencia, Spain.
Francisco García-GarcíaBioinformatics & Biostatistics Unit, Prince Felipe Research Center, Valencia, Spain.ORCID 0000-0001-8354-5636
Consuelo GuerriMolecular and cellular pathology of Alcohol Laboratory, Prince Felipe Research Center, Valencia, Spain.
Centro de Investigacion Principe Felipe · ESFundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TLR4 is a member of the toll-like receptors (TLR) immune family, which are activated by lipopolysaccharide, ethanol or damaged tissue, among others, by triggering proinflammatory cytokines release and inflammation. Lack of TLR4 protects against inflammatory processes and neuroinflammation linked with several neuropathologies. By considering that miRNAs are key post-transcriptional regulators of the proteins involved in distinct cellular processes, including inflammation, this study aimed to assess the impact of the miRNAs profile in mice cortices lacking the TLR4 response. Using mice cerebral cortices and next-generation sequencing (NGS), the findings showed that lack of TLR4 significantly reduced the quantity and diversity of the miRNAs expressed in WT mice cortices. The results also revealed a significant down-regulation of the miR-200 family, while cluster miR-99b/let-7e/miR-125a was up-regulated in TLR4-KO vs. WT. The bioinformatics and functional analyses demonstrated that TLR4-KO presented the systematic depletion of many pathways closely related to the immune system response, such as cytokine and interleukin signaling, MAPK and ion Channels routes, MyD88 pathways, NF-κβ and TLR7/8 pathways. Our results provide new insights into the molecular and biological processes associated with the protective effects of TLR-KO against inflammatory damage and neuroinflammation, and reveal the relevance of the TLR4 receptors response in many neuropathologies.

Indexed as

AnimalsCerebral CortexCytokinesFemaleGene Expression RegulationInflammationLipopolysaccharidesMiceMice, Inbred C57BLMice, KnockoutMicroRNAsSignal TransductionToll-Like Receptor 4TranscriptomeCytokinesLipopolysaccharidesMicroRNAsMirn200 microRNA, mouseMirn99 microRNA, mouseTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID32780740
PMCPMC7418977
OpenAlexW3048514197

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.