Evidence map›Paper›PMID 32994523›Full record

ArticleScientific reports2020

miR-369-3p modulates inducible nitric oxide synthase and is involved in regulation of chronic inflammatory response.

Viviana Scalavino, Marina Liso, Elisabetta Cavalcanti, Isabella Gigante, Antonio Lippolis, Mauro Mastronardi, Marcello Chieppa, Grazia Serino

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.9field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 51 citations in OpenAlex.

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  3. Mechanisms ofBreathe (Sheffield, England) · 2026
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  17. Pathogens (Basel, Switzerland) · 2024
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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

8 authors at 1 institution in 1 country.

Viviana Scalavino *National Institute of Gastroenterology "S. de Bellis", Research Hospital, Via Turi, 27, Castellana Grotte, 70013, Bari, Italy.
Marina Liso *National Institute of Gastroenterology "S. de Bellis", Research Hospital, Via Turi, 27, Castellana Grotte, 70013, Bari, Italy.
Elisabetta CavalcantiNational Institute of Gastroenterology "S. de Bellis", Research Hospital, Via Turi, 27, Castellana Grotte, 70013, Bari, Italy.
Isabella GiganteNational Institute of Gastroenterology "S. de Bellis", Research Hospital, Via Turi, 27, Castellana Grotte, 70013, Bari, Italy.
Antonio LippolisNational Institute of Gastroenterology "S. de Bellis", Research Hospital, Via Turi, 27, Castellana Grotte, 70013, Bari, Italy.
Mauro MastronardiNational Institute of Gastroenterology "S. de Bellis", Research Hospital, Via Turi, 27, Castellana Grotte, 70013, Bari, Italy.
Marcello ChieppaNational Institute of Gastroenterology "S. de Bellis", Research Hospital, Via Turi, 27, Castellana Grotte, 70013, Bari, Italy.
Grazia SerinoNational Institute of Gastroenterology "S. de Bellis", Research Hospital, Via Turi, 27, Castellana Grotte, 70013, Bari, Italy. grazia.serino@irccsdebellis.it.ORCID http://orcid.org/0000-0002-2971-0802
Gastroenterology Hospital "Saverio de Bellis" · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dendritic cells are the most important antigen-presenting cells that link the innate and acquired immune system. In our previous study, we identified that the upregulation of miR-369-3p suppresses the LPS-induced inflammatory response, reducing C/EBP-β, TNFα and IL-6 production. With the aim of gaining further insight into the biological function of miR-369-3p during acute inflammatory response, in the present study we identified novel gene targets of miR-369-3p and demonstrated the suppressive ability of these genes on the inflammatory dendritic cells. Bioinformatic analyses revealed that iNOS is a potential target of miR-369-3p. We demonstrated that the ectopic induction of miR-369-3p markedly reduced iNOS mRNA and protein as well as NO production. Moreover, we found that the upregulation of miR-369-3p decreased the release of TNFα, IL-6, IL-12, IL-1α, IL-1β in response to LPS, and increased the production of anti-inflammatory cytokines such as IL-10 and IL-1RA. In addition, LPS-induced nuclear translocation of NF-kB was inhibited by miR-369-3p. Levels of miR-369-3p were decreased in human inflamed regions of human intestine obtained from IBD patients. Our results provide novel additional information on miR-369-3p as a potential core of the signaling regulating the inflammatory response. These findings suggest that miR-369-3p should be considered as a potential target for the future development of new molecular therapeutic approaches.

Indexed as

AnimalsCCAAT-Enhancer-Binding Protein-betaCytokinesDendritic CellsInflammationInterleukin-12Interleukin-6LipopolysaccharidesMaleMiceMice, Inbred C57BLMicroRNAsNF-kappa BNitric OxideNitric Oxide Synthase Type IISignal TransductionCCAAT-Enhancer-Binding Protein-betaCytokinesInterleukin-12Interleukin-6LipopolysaccharidesMicroRNAsMIRN369 microRNA, mouseNF-kappa BNitric OxideNitric Oxide Synthase Type IITumor Necrosis Factor-alpha

Identifiers

PMID32994523
PMCPMC7525504
OpenAlexW3089763322

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.