Evidence map›Paper›PMID 24628936›Full record

ArticleCell communication and signaling : CCS2014

Activin A induces growth arrest through a SMAD- dependent pathway in hepatic progenitor cells.

Lin Chen, Wei Zhang, Hui-fang Liang, Qiao-fan Zhou, Ze-yang Ding, Hong-qiang Yang, Wei-bo Liu, Yan-hui Wu, Quan Man, Bi-xiang Zhang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. The Role of Autophagy for the Regeneration of the Aging Liver.International journal of molecular sciences · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Endothelial transcription factor KLF2 negatively regulates liver regeneration via induction of activin A.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  13. Review
  14. Article
  15. Article
  16. HBx interacted with Smad4 to deprive activin a growth inhibition function in hepatocyte HL7702 on CRM1 manner.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  17. Review
  18. Article
  19. Suberoylanilide hydroxamic acid enhances chemosensitivity to 5-fluorouracil in hepatocellular carcinoma via inhibition of thymidylate synthase.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  20. Article
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

11 authors at 2 institutions in 1 country.

Lin Chen
Wei Zhang
Hui-fang Liang
Qiao-fan Zhou
Ze-yang Ding
Hong-qiang Yang
Wei-bo Liu
Yan-hui Wu
Quan Man
Bi-xiang Zhang
Xiao-ping ChenHepatic surgery centre, Tongji Medical College, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China. chenxp@medmail.com.cn.
Tongji Hospital · CNFirst Affiliated Hospital of Shihezi University Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundActivin A, an important member of transforming growth factor-β superfamily, is reported to inhibit proliferation of mature hepatocyte. However, the effect of activin A on growth of hepatic progenitor cells is not fully understood. To that end, we attempted to evaluate the potential role of activin A in the regulation of hepatic progenitor cell proliferation.

resultsUsing the 2-acetaminofluorene/partial hepatectomy model, activin A expression decreased immediately after partial hepatectomy and then increased from the 9th to 15th day post surgery, which is associated with the attenuation of oval cell proliferation. Activin A inhibited oval cell line LE6 growth via activating the SMAD signaling pathway, which manifested as the phosphorylation of SMAD2/3, the inhibition of Rb phosphorylation, the suppression of cyclinD1 and cyclinE, and the promotion of p21WAF1/Cip1 and p15INK4B expression. Treatment with activin A antagonist follistatin or blocking SMAD signaling could diminish the anti-proliferative effect of activin A. By contrast, inhibition of the MAPK pathway did not contribute to this effect. Antagonizing activin A activity by follistatin administration enhanced oval cell proliferation in the 2-acetylaminofluorene/partial hepatectomy model.

conclusionActivin A, acting through the SMAD pathway, negatively regulates the proliferation of hepatic progenitor cells.

Indexed as

Cell ProliferationActivinsAnimalsCell LineCyclin D1Cyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p21Cyclin EFollistatinHepatocytesRatsSignal TransductionSmad ProteinsStem Cellsactivin AActivinsCdkn1a protein, ratCyclin D1Cyclin-Dependent Kinase Inhibitor p15Cyclin-Dependent Kinase Inhibitor p21Cyclin EFollistatinSmad Proteins

Identifiers

PMID24628936
PMCPMC3995548
OpenAlexW2110688790

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.