Evidence map›Paper›PMID 33109608›Full record

ArticleThe Journal of biological chemistry2020

Transcription factor NF-κB promotes acute lung injury

Jie Zhao, Fei Xie, Ruidong Chen, Zhen Zhang, Rujun Dai, Na Zhao, Rongxin Wang, Yanhong Sun, Yue Chen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 22 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

9 authors at 1 institution in 1 country.

Jie ZhaoThe Second Department of Pediatric, Cangzhou Central Hospital, Cangzhou, P. R. China. Electronic address: zhaojie601906726@163.com.
Fei XieThe Six Department of Pediatric, Cangzhou Central Hospital, Cangzhou, P. R. China.
Ruidong ChenThe Six Department of Pediatric, Cangzhou Central Hospital, Cangzhou, P. R. China.
Zhen ZhangThe Second Department of Pediatric, Cangzhou Central Hospital, Cangzhou, P. R. China.
Rujun DaiThe Second Department of Pediatric, Cangzhou Central Hospital, Cangzhou, P. R. China.
Na ZhaoThe Second Department of Pediatric, Cangzhou Central Hospital, Cangzhou, P. R. China.
Rongxin WangThe Second Department of Pediatric, Cangzhou Central Hospital, Cangzhou, P. R. China.
Yanhong SunThe Second Department of Pediatric, Cangzhou Central Hospital, Cangzhou, P. R. China.
Yue ChenThe Second Department of Pediatric, Cangzhou Central Hospital, Cangzhou, P. R. China.
Cangzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute lung injury (ALI), is a rapidly progressing heterogenous pulmonary disorder that possesses a high risk of mortality. Accumulating evidence has implicated the activation of the p65 subunit of NF-κB [NF-κB(p65)] activation in the pathological process of ALI. microRNAs (miRNAs), a group of small RNA molecules, have emerged as major governors due to their post-transcriptional regulation of gene expression in a wide array of pathological processes, including ALI. The dysregulation of miRNAs and NF-κB activation has been implicated in human diseases. In the current study, we set out to decipher the convergence of miR-99b and p65 NF-κB activation in ALI pathology. We measured the release of pro-inflammatory cytokines (IL-1β, IL-6, and TNFα) in bronchoalveolar lavage fluid using ELISA. MH-S cells were cultured and their viability were detected with cell counting kit 8 (CCK8) assays. The results showed that miR-99b was up-regulated, while PRDM1 was down-regulated in a lipopolysaccharide (LPS)-induced murine model of ALI. Mechanistic investigations showed that NF-κB(p65) was enriched at the miR-99b promoter region, and further promoted its transcriptional activity. Furthermore, miR-99b targeted PRDM1 by binding to its 3'UTR, causing its down-regulation. This in-creased lung injury, as evidenced by increased wet/dry ratio of mouse lung, myeloperoxidase activity and pro-inflammatory cytokine secretion, and enhanced infiltration of inflammatory cells in lung tissues. Together, our findings indicate that NF-κB(p65) promotion of miR-99b can aggravate ALI in mice by down-regulating the expression of PRDM1.

Indexed as

Gene Expression RegulationAcute Lung InjuryAnimalsLipopolysaccharidesMaleMiceMice, Inbred C57BLMicroRNAsNF-kappa BPositive Regulatory Domain I-Binding Factor 1Signal TransductionLipopolysaccharidesMicroRNAsMirn99 microRNA, mouseNF-kappa BPositive Regulatory Domain I-Binding Factor 1Prdm1 protein, mouseacute lung injurycell biologycell cyclecell deathinflammatory factorslunglung injurymicroRNA-99bNF-kB(p65)NF-κB(p65, )PRDM1

Identifiers

PMID33109608
PMCPMC7939479
OpenAlexW3097151069

What OpenQuestion holds

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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.