Evidence map›Paper›PMID 34092219›Full record

ArticleBMC pulmonary medicine2021

Down-regulation of SNHG16 alleviates the acute lung injury in sepsis rats through miR-128-3p/HMGB3 axis.

Junli Sun, Keke Xin, Chenghui Leng, Jianlin Ge

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.2field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  5. Structure and Functions of HMGB3 Protein.International journal of molecular sciences · 2024
    Review
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  10. Isoliquiritigenin regulates the circ_0002860/miR-431-5p/RAB9A axis to function as a tumor inhibitor in melanoma.The journal of venomous animals and toxins including tropical diseases · 2023
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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 1 institution in 1 country.

Junli SunGeneral ICU, Luoyang Central Hospital Affiliated To Zhengzhou University, 288 Zhongzhou Middle Road, Luoyang, 471009, Henan, China. li14688331932@163.com.
Keke XinGeneral ICU, Luoyang Central Hospital Affiliated To Zhengzhou University, 288 Zhongzhou Middle Road, Luoyang, 471009, Henan, China.
Chenghui LengGeneral ICU, Luoyang Central Hospital Affiliated To Zhengzhou University, 288 Zhongzhou Middle Road, Luoyang, 471009, Henan, China.
Jianlin GeGeneral ICU, Luoyang Central Hospital Affiliated To Zhengzhou University, 288 Zhongzhou Middle Road, Luoyang, 471009, Henan, China.
Luoyang Central Hospital Affiliated to Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong noncoding RNAs contribute to various inflammatory diseases, including sepsis. We explore the role of small nucleolar RNA host gene 16 (SNHG16) in sepsis-mediated acute lung injury (ALI) and inflammation.

methodsA sepsis-induced ALI rat model was constructed by the cecal ligation and perforation method. The profiles of SNHG16, miR-128-3p, and high-mobility group box 3 (HMGB3) were monitored by quantitative reverse transcription PCR and Western blot. The pathologic changes of lung tissues were evaluated by Hematoxylin-Eosin staining, immunohistochemistry, and dry and wet method. Meanwhile, the pro-inflammatory factors and proteins were determined by ELISA and Western blot. In contrast, a sepsis model in BEAS-2B was induced with lipopolysaccharide (LPS) to verify the effects of SNHG16/miR-128-3p/HMGB3 on lung epithelial cell viability and apoptosis.

resultsAs a result, SNHG16 and HMGB3 were up-regulated, while miR-128-3p was down-regulated in sepsis-induced ALI both in vivo and in vitro. Inhibiting SNHG16 reduced the apoptosis and inflammation in the sepsis-induced ALI model. Overexpressing SNHG16 promoted LPS-mediated lung epithelial apoptosis and inhibited cell viability and inflammation, while miR-128-3p had the opposite effects. Mechanistically, SNHG16 targeted miR-128-3p and attenuated its expression, while miR-128-3p targeted the 3' untranslated region of HMGB3.

conclusionsOverall, down-regulating SNHG16 alleviated the sepsis-mediated ALI by regulating miR-128-3p/HMGB3.

Indexed as

Acute Lung InjuryAnimalsApoptosisCell SurvivalDown-RegulationGene Expression RegulationHMGB3 ProteinHumansLipopolysaccharidesMaleMicroRNAsRatsRats, Sprague-DawleyRNA, Long NoncodingSepsisUp-RegulationHMGB3 ProteinLipopolysaccharidesMicroRNAsMIRN128 microRNA, ratRNA, Long NoncodingAcute lung injuryApoptosisInflammatory responseSepsisSNHG16

Identifiers

PMID34092219
PMCPMC8180123
OpenAlexW3167778059

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LicenceCC BY
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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.