Evidence map›Paper›PMID 28902846›Full record

ArticlePloS one2017

Downregulation of microRNA-145 may contribute to liver fibrosis in biliary atresia by targeting ADD3.

Yongqin Ye, Zhihan Li, Qi Feng, Zimin Chen, Zhouguang Wu, Jianyao Wang, Xiaoshuo Ye, Dahao Zhang, Lei Liu, Wei Gao and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
3.5field-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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Genetic background and biliary atresia.World journal of pediatric surgery · 2025
    Review
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  10. Contribution ofInternational journal of molecular sciences · 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

12 authors at 5 institutions in 1 country.

Yongqin YeShantou University Medical College, Shantou, Guangdong, China.
Zhihan LiShantou University Medical College, Shantou, Guangdong, China.
Qi FengDepartment of General Surgery, Shenzhen Children's Hospital, Shenzhen, Guangdong, China.
Zimin ChenDepartment of General Surgery, Shenzhen Children's Hospital, Shenzhen, Guangdong, China.
Zhouguang WuDepartment of General Surgery, Shenzhen Children's Hospital, Shenzhen, Guangdong, China.
Jianyao WangDepartment of General Surgery, Shenzhen Children's Hospital, Shenzhen, Guangdong, China.
Xiaoshuo YeDepartment of General Surgery, Shenzhen Children's Hospital, Shenzhen, Guangdong, China.
Dahao ZhangShantou University Medical College, Shantou, Guangdong, China.
Lei LiuShenzhen Key Laboratory of Hepatobiliary Disease, Shenzhen Third People's Hospital, Shenzhen, Guangdong, China.
Wei GaoDepartment of Organ Transplatation, Tianjin First Center Hospital, Tianjin, China.
Lihui ZhangDepartment of Traditional Chinese Medicine, Shenzhen Children's Hospital, Shenzhen, Guangdong, China.
Bin WangDepartment of General Surgery, Shenzhen Children's Hospital, Shenzhen, Guangdong, China.
Shenzhen Children's Hospital · CNShantou University · CNShantou University Medical College · CNShenzhen Third People’s Hospital · CNTianjin First Center Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesBiliary atresia (BA) is a pediatric liver disease characterized by fibro-obliteration and obstruction of the extrahepatic biliary system, that invariably leads to cirrhosis and even death, if left untreated for extended time. However, its pathology and etiology still remained unknown. In this study, we tested the expression of adducin 3 (ADD3), the gene identified as a susceptibility gene in BA by GWAS, and uncovered its upstream regulatory microRNA in the pathogenesis of BA.

methodsIn this study, 14 infants with BA and 14 infants with choledochal cyst (CC) were enrolled as experimental group and control group, respectively. ADD3 and microRNA-145 (miR-145) expression profiles in liver tissues of BA and CC were determined using qPCR. Luciferase reporter assay was performed to verify the direct interaction between miR-145-5p and ADD3 3' Untranslated Regions (3'UTR). The Lentiviral vectors containing miR-145, miR-145-3p inhibitor, miR-145-5p inhibitor, empty vector were transfected into human hepatic stellate cell line (LX-2) to determine the functional effect of miR-145 on ADD3 expression at both mRNA and protein level.

resultsMiR-145 was shown to be down-regulated in liver tissues of infants with BA compared to CC (p = 0.0267). ADD3, verified as a target of miR-145-5p, was shown to be overexpressed in infants with BA at the mRNA level (p = 0.0118). Transfection of lentiviruses containing miR-145 into LX-2 cells decreased the expression of ADD3 at both mRNA and protein level compared to negative control group, and suppressed the expression of p-Akt at protein level.

conclusionsOur study has shown that overexpressed ADD3 and downregulated miR-145 were detected in BA liver tissues. MiR-145-5p was confirmed to target ADD3 by luciferase reporter assay. The downregulation of miR-145 may contribute to liver fibrosis in BA by upregulating the expression of ADD3.

Indexed as

AdducinsBiliary AtresiaCalmodulin-Binding ProteinsCase-Control StudiesCells, CulturedDown-RegulationFemaleGene Expression RegulationHumansInfantLiver CirrhosisMaleMicroRNAsRetrospective StudiesADD3 protein, humanAdducinsCalmodulin-Binding ProteinsMicroRNAsMIRN145 microRNA, human

Identifiers

PMID28902846
PMCPMC5597134
OpenAlexW2754728593

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.