Evidence map›Paper›PMID 34126975›Full record

ArticleBMC pulmonary medicine2021

Long non-coding RNA CDKN2B-AS1 enhances LPS-induced apoptotic and inflammatory damages in human lung epithelial cells via regulating the miR-140-5p/TGFBR2/Smad3 signal network.

Bing Wang, Qi Sun, Wen Ye, Lianghai Li, Ping Jin

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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 32% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Bing Wang *Department of Intensive Care Unit, The Second Clinical Medical College, Jingzhou Central Hospital, Yangtze University, No. 1 Renmin Road, Jingzhou District, Jingzhou, 434000, Hubei, China.
Qi Sun *Department of Intensive Care Unit, The Second Clinical Medical College, Jingzhou Central Hospital, Yangtze University, No. 1 Renmin Road, Jingzhou District, Jingzhou, 434000, Hubei, China.
Wen YeBlood Purification Center, The Second Clinical Medical College, Jingzhou Central Hospital, Yangtze University, Jingzhou, 434000, Hubei, China.
Lianghai LiDepartment of Intensive Care Unit, The Second Clinical Medical College, Jingzhou Central Hospital, Yangtze University, No. 1 Renmin Road, Jingzhou District, Jingzhou, 434000, Hubei, China.
Ping JinDepartment of Intensive Care Unit, The Second Clinical Medical College, Jingzhou Central Hospital, Yangtze University, No. 1 Renmin Road, Jingzhou District, Jingzhou, 434000, Hubei, China. iceking123456789@163.com.
Jingzhou Central Hospital · CNYangtze University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSepsis is a complicated disease with systemic inflammation or organ dysfunction, and it is the leading cause of acute lung injury (ALI). Long non-coding RNAs (lncRNAs) have played important roles in the pathogenesis of sepsis. This study was designed to explore the biological function and regulatory mechanism of cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) in lipopolysaccharide (LPS)-induced lung injury.

methodsALI model was established after human lung epithelial cell line BEAS-2B was exposed to LPS. CDKN2B-AS1, microRNA-140-5p (miR-140-5p) and transforming Growth Factor Beta Receptor II (TGFBR2) levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was measured using Cell Counting Kit-8 (CCK-8). Cell apoptosis was assessed by caspase3 activity and flow cytometry. Inflammatory cytokines were examined via enzyme-linked immunosorbent assay (ELISA). Protein analysis was performed through western blot. Dual-luciferase reporter, RNA immunoprecipitation (RIP) and pull-down assays were applied to validate the interaction between targets.

resultsCDKN2B-AS1 and TGFBR2 were abnormally upregulated in sepsis patients. Functionally, CDKN2B-AS1 or TGFBR2 knockdown promoted cell growth but inhibited cell apoptosis and inflammatory response in LPS-treated BEAS-2B cells. Moreover, the regulation of CDKN2B-AS1 in LPS-induced cell injury was achieved by increasing the TGFBR2 expression. CDKN2B-AS1 was identified as a miR-140-5p sponge and TGFBR2 was a target of miR-140-5p. Furthermore, CDKN2B-AS1 could regulate the TGFBR2/Smad3 pathway by sponging miR-140-5p.

conclusionsThese results suggested that CDKN2B-AS1 contributed to the LPS-mediated apoptosis and inflammation in BEAS-2B cells via the miR-140-5p/TGFBR2/Smad3 axis.

Indexed as

Acute Lung InjuryApoptosisCell Line, TumorCell SurvivalEpithelial CellsFemaleHumansLipopolysaccharidesLungMaleMicroRNAsMiddle AgedReceptor, Transforming Growth Factor-beta Type IIRNA, Long NoncodingSignal TransductionSmad3 ProteinCDKN2B antisense RNA, humanLipopolysaccharidesMicroRNAsMirn140 microRNA, humanReceptor, Transforming Growth Factor-beta Type IIRNA, Long NoncodingSmad3 ProteinSMAD3 protein, humanTGFBR2 protein, humanAcute lung injuryCDKN2B-AS1miR-140-5pSepsisSmad3TGFBR2

Identifiers

PMID34126975
PMCPMC8201744
OpenAlexW3166932330

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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.