Evidence map›Paper›PMID 21931759›Full record

ArticlePloS one2011

Hepatocyte growth factor (HGF) inhibits collagen I and IV synthesis in hepatic stellate cells by miRNA-29 induction.

Monika Kwiecinski, Andrea Noetel, Natalia Elfimova, Jonel Trebicka, Stephanie Schievenbusch, Ingo Strack, Levente Molnar, Melanie von Brandenstein, Ulrich Töx, Roswitha Nischt and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
8.3field-weighted citation impact, top 1% 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

83 citing papers in PubMed, 151 citations in OpenAlex.

  1. Review
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  3. PlacentaAmerican journal of physiology. Endocrinology and metabolism · 2025
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  19. PGC1α suppresses kidney cancer progression by inhibiting collagen-induced SNAIL expression.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Article
  20. Article

23 more citing papers are in PubMed but not listed here.

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

13 authors at 2 institutions in 1 country.

Monika KwiecinskiInstitute for Pathology, University Hospital Cologne, Cologne, Germany.
Andrea Noetel
Natalia Elfimova
Jonel Trebicka
Stephanie Schievenbusch
Ingo Strack
Levente Molnar
Melanie von Brandenstein
Ulrich Töx
Roswitha Nischt
Oliver Coutelle
Hans Peter Dienes
Margarete Odenthal
University Hospital Cologne · DEUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn chronic liver disease, hepatic stellate cells (HSC) transdifferentiate into myofibroblasts, promoting extracellular matrix (ECM) synthesis and deposition. Stimulation of HSC by transforming growth factor-β (TGF-β) is a crucial event in liver fibrogenesis due to its impact on myofibroblastic transition and ECM induction. In contrast, hepatocyte growth factor (HGF), exerts antifibrotic activities. Recently, miR-29 has been reported to be involved in ECM synthesis. We therefore studied the influence of HGF and TGF-β on the miR-29 collagen axis in HSC. METHODOLOGY: HSC, isolated from rats, were characterized for HGF and Met receptor expression by Real-Time PCR and Western blotting during culture induced myofibroblastic transition. Then, the levels of TGF-β, HGF, collagen-I and -IV mRNA, in addition to miR-29a and miR-29b were determined after HGF and TGF-β stimulation of HSC or after experimental fibrosis induced by bile-duct obstruction in rats. The interaction of miR-29 with 3'-untranslated mRNA regions (UTR) was analyzed by reporter assays. The repressive effect of miR-29 on collagen synthesis was studied in HSC treated with miR-29-mimicks by Real-Time PCR and immunoblotting. PRINCIPAL

findingsThe 3'-UTR of the collagen-1 and -4 subtypes were identified to bind miR-29. Hence, miR-29a/b overexpression in HSC resulted in a marked reduction of collagen-I and -IV synthesis. Conversely, a decrease in miR-29 levels is observed during collagen accumulation upon experimental fibrosis, in vivo, and after TGF-β stimulation of HSC, in vitro. Finally, we show that during myofibroblastic transition and TGF-β exposure the HGF-receptor, Met, is upregulated in HSC. Thus, whereas TGF-β stimulation leads to a reduction in miR-29 expression and de-repression of collagen synthesis, stimulation with HGF was definitely associated with highly elevated miR-29 levels and markedly repressed collagen-I and -IV synthesis.

conclusionsUpregulation of miRNA-29 by HGF and downregulation by TGF-β take part in the anti- or profibrogenic response of HSC, respectively.

Indexed as

3' Untranslated RegionsAnimalsBile DuctsCell DifferentiationCollagen Type ICollagen Type IVComputational BiologyExtracellular MatrixFibroblastsFibrosisHepatic Stellate CellsHepatocyte Growth FactorMaleMicroRNAsProto-Oncogene Proteins c-metRats3' Untranslated RegionsCollagen Type ICollagen Type IVHepatocyte Growth FactorMicroRNAsMIRN29 microRNA, ratProto-Oncogene Proteins c-metRNA, MessengerTransforming Growth Factor beta

Identifiers

PMID21931759
PMCPMC3170366
OpenAlexW1965895613

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LicenceCC BY
Read underepoch 390

Registered trials

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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.