Evidence map›Paper›PMID 20110463›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2010

miR-221 suppresses ICAM-1 translation and regulates interferon-gamma-induced ICAM-1 expression in human cholangiocytes.

Guoku Hu, Ai-Yu Gong, Jun Liu, Rui Zhou, Caishu Deng, Xian-Ming Chen

Abstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed, 60 citations in OpenAlex.

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  15. Central nervous system niche involvement in the leukemia.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2016
    Review
  16. Article
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  18. IFN-α-Induced Downregulation of miR-221 in Dendritic Cells: Implications for HCV Pathogenesis and Treatment.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2015
    Article
  19. Review
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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 1 institution in 1 country.

Guoku HuDepartment of Medical Microbiology and Immunology, Creighton University Medical Center, Omaha, Nebraska 68178, USA.
Ai-Yu Gong
Jun Liu
Rui Zhou
Caishu Deng
Xian-Ming Chen
CHI Health Creighton University Medical Center - Bergan Mercy · US

Funding

MicroRNAs in Epithelial Innate Immunity to C. parvumR01AI071321 · NIAID · MAYO CLINIC ROCHESTER · PI CHEN, XIAN-MING · 2006 to 2010
$1.3M
NIAID NIH HHS AI071321NIAID NIH HHS R01 AI071321
6 · The paper itself

Abstract

Aberrant cholangiocyte reactions in response to inflammatory stimuli are important pathogenic factors for the persistent biliary inflammation in patients with cholangiopathies. Overexpression of intercellular cell adhesion molecule-1 (ICAM-1) in cholangiocytes is a common pathological feature in inflammatory cholangiopathies and can promote cholangiocyte interactions with effector lymphocytes in the portal region. In this study, we tested the involvement of miRNA-mediated posttranscriptional regulation in IFN-gamma-induced ICAM-1 expression in cholangiocytes. Using both immortalized and nonimmortalized human cholangiocyte cell lines, we found that IFN-gamma activated ICAM-1 transcription and increased ICAM-1 protein expression. Inhibition of ICAM-1 transcription could only partially block IFN-gamma-induced ICAM-1 expression at the protein level. In silico target prediction analysis revealed complementarity of miR-221 to the 3'-untranslated region of ICAM-1 mRNA. Targeting of ICAM-1 3'-untranslated region by miR-221 resulted in translational repression in cholangiocytes but not ICAM-1 mRNA degradation. Functional inhibition of miR-221 with anti-miR-221 induced ICAM-1 protein expression. Moreover, IFN-gamma stimulation decreased miR-221 expression in cholangiocytes in a signal transducer and activator of transcription 1-dependent manner. Transfection of miR-221 precursor abolished IFN-gamma-stimulated ICAM-1 protein expression. In addition, miR-221-mediated expression of ICAM-1 on cholangiocytes showed a significant influence on the adherence of cocultured T cells. These findings indicate that both transcriptional and miRNA-mediated posttranscriptional mechanisms are involved in IFN-gamma-induced ICAM-1 expression in human cholangiocytes, suggesting an important role for miRNAs in the regulation of cholangiocyte inflammatory responses.

Indexed as

3' Untranslated RegionsBile DuctsCell AdhesionCell Line, TransformedCell SurvivalDactinomycinDown-RegulationEpithelial CellsGene Expression RegulationGenes, ReporterHumansIntercellular Adhesion Molecule-1Interferon-gammaJurkat CellsMicroRNAsMutation3' Untranslated RegionsDactinomycinIntercellular Adhesion Molecule-1Interferon-gammaMicroRNAsMIR221, humanRNA, Small InterferingSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID20110463
PMCPMC2853302
OpenAlexW2156375236

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.