Evidence map›Paper›PMID 26437572›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2015

MicroRNA-34a Promotes Hepatic Stellate Cell Activation via Targeting ACSL1.

Gangli Yan, Binbin Li, Xuan Xin, Midie Xu, Guoqing Ji, Hongyu Yu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  8. Article
  9. Up-regulation of miR-34b/c by JNK and FOXO3 protects from liver fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. Review
  11. Review
  12. Article
  13. miRNA Signature in NAFLD: A Turning Point for a Non-Invasive Diagnosis.International journal of molecular sciences · 2018
    Review
  14. The Role of miRNAs in the Pathophysiology of Liver Diseases and Toxicity.International journal of molecular sciences · 2018
    Review
  15. Article
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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

6 authors at 2 institutions in 1 country.

Gangli YanDepartment of Pathology, Changzheng Hospital, The Second Military Medical University, Shanghai, China (mainland).
Binbin LiDepartment of Pathology, Changzheng Hospital, The Second Military Medical University, Shanghai, China (mainland).
Xuan XinDepartment of Pathology, Changzheng Hospital, The Second Military Medical University, Shanghai, China (mainland).
Midie XuDepartment of Pathology, Changzheng Hospital,the Second Military Medical University, Shanghai, China (mainland).
Guoqing JiState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai, China (mainland).
Hongyu YuDepartment of Pathology, Changzheng Hospital, The Second Military Medical University, Shanghai, China (mainland).
Second Military Medical University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe incidence of liver fibrosis remains high due to the lack of effective therapies. Our previous work found that microRNA (miR)-34a expression was increased, while acy1-CoA synthetase long-chain family member1 (ACSL1) was decreased, in a dimethylnitrosamine (DNS)-induced hepatic fibrosis rat model. We hypothesized that miR-34a may play a role in the process of hepatic fibrosis by targeting ACSL1. MATERIAL AND

methodsFrom days 2 to 14, cultured primary hepatic stellate cells (HSCs) underwent cell morphology, immunocytochemical staining, and quantitative reverse transcription PCR (RT-qPCR) for alpha smooth muscle actin (a-SMA), desmin, rno-miR-34a, and ACSL1 expression. Wild-type and mutant luciferase reporter plasmids were constructed according to the predicted miR-34a binding site on the 3'-untranslated region (UTR) of the ACSL1 mRNA and then transfected into HEK293 cells. rno-miR-34a was silenced in HSCs to confirm that rno-miR-34a negatively regulates ACSL1 expression. mRNA and protein expression of α-SMA, type I collagen, and desmin were assayed in miR-34a-silenced HSCs.

resultsHSCs were deemed quiescent during the first 3 days and activated after 10 days. rno-miR-34a expression increased, and ACSL1 expression decreased, from day 2 to 7 to 14. rno-miR-34a was shown to specifically bind to the 3'-UTR of ACSL1. miR-34a-silenced HSCs showed higher ACSL1and lower α-SMA, type I collagen, and desmin expression than that of matching negative controls and non-transfected cells.

conclusionsmiR-34a appears to play an important role in the process of liver fibrosis by targeting ACSL1 and may show promise as a therapeutic molecular target for hepatic fibrosis.

Indexed as

Gene Expression Regulation3' Untranslated RegionsActinsAnimalsBasic Helix-Loop-Helix ProteinsDimethylnitrosamineGene SilencingHEK293 CellsHepatic Stellate CellsHumansImmunohistochemistryLiverLiver CirrhosisMaleMicroRNAsRats3' Untranslated RegionsActinsASCL1 protein, humanAscl1 protein, ratBasic Helix-Loop-Helix ProteinsDimethylnitrosamineMicroRNAsMIRN34 microRNA, humanMIRN34 microRNA, rat

Identifiers

PMID26437572
PMCPMC4601392
OpenAlexW2203200063

What OpenQuestion holds

Textmetadata
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.