Evidence map›Paper›PMID 29167424›Full record

ArticleScientific reports2017

MiR-92a and miR-486 are potential diagnostic biomarkers for mercury poisoning and jointly sustain NF-κB activity in mercury toxicity.

Enmin Ding, Jun Guo, Ying Bai, Hengdong Zhang, Xin Liu, Wenyan Cai, Lixin Zhong, Baoli Zhu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

7 citing papers in PubMed, 24 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

8 authors at 2 institutions in 1 country.

Enmin DingInstitute of Occupational Disease Prevention, Jiangsu Provincial Center for Disease Prevention and Control, Nanjing, Jiangsu Province, People's Republic of China.
Jun GuoYandu District Center for Disease Prevention and Control, YanCheng, Jiangsu Province, People's Republic of China.
Ying BaiInstitute of Occupational Disease Prevention, Jiangsu Provincial Center for Disease Prevention and Control, Nanjing, Jiangsu Province, People's Republic of China.
Hengdong ZhangInstitute of Occupational Disease Prevention, Jiangsu Provincial Center for Disease Prevention and Control, Nanjing, Jiangsu Province, People's Republic of China.
Xin LiuInstitute of Occupational Disease Prevention, Jiangsu Provincial Center for Disease Prevention and Control, Nanjing, Jiangsu Province, People's Republic of China.
Wenyan CaiSchool of Public Health, Nanjing Medical University, Nanjing, Jiangsu Province, People's Republic of China.
Lixin ZhongInstitute of Occupational Disease Prevention, Jiangsu Provincial Center for Disease Prevention and Control, Nanjing, Jiangsu Province, People's Republic of China.
Baoli ZhuInstitute of Occupational Disease Prevention, Jiangsu Provincial Center for Disease Prevention and Control, Nanjing, Jiangsu Province, People's Republic of China. zhubl@jscdc.cn.
Jiangsu Provincial Center for Disease Control and Prevention · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Occupational and environmental exposure to mercury is a public health concern worldwide. Although the altered epigenetic regulatory features, such as microRNA, have been associated with mercury exposure, the underlying molecular mechanism is not well illuminated. This study aimed to confirm that hsa-miR-92a and hsa-miR-486 are novel diagnostic biomarkers of occupational mercury poisoning, and to explore the underlying mechanism of miR-92a and miR-486 in mercury toxicity. RT-qPCR assays and receiver operating characteristics curve analyses were conducted to confirm the diagnostic value of miR-92a and miR-486 as biomarkers of occupational mercury poisoning. Dual-luciferase assay was applied to confirm the target gene of miR-92a and miR-486 in vitro. Then, we established an in-vitro model where miR-92a and miR-486 were overexpressed or knocked down in HEK-293 and HUVEC cells. RT-qPCR and western blotting were used to analyze gene and protein expression levels. Cell apoptosis was determined by flow cytometry. Results show that miR-92a and miR-486 expression levels were up-regulated in workers exposed to occupational mercury. Upregulation of miR-92a and miR-486 may play a crucial role in mercury toxicity by jointly activating the NF-κB signaling pathway via targeting KLF4 and Cezanne, respectively.

Indexed as

BiomarkersBlotting, WesternHEK293 CellsHumansHuman Umbilical Vein Endothelial CellsKruppel-Like Factor 4Mercury PoisoningMicroRNAsNF-kappa BSignal TransductionBiomarkersKLF4 protein, humanKruppel-Like Factor 4MicroRNAsMIRN486 microRNA, humanMIRN92 microRNA, humanNF-kappa B

Identifiers

PMID29167424
PMCPMC5700070
OpenAlexW2769804791

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.