Evidence map›Paper›PMID 18385520›Full record

ArticleThe American journal of pathology2008

Deletion of the Met tyrosine kinase in liver progenitor oval cells increases sensitivity to apoptosis in vitro.

Gaelle del Castillo, Valentina M Factor, Margarita Fernández, Alberto Alvarez-Barrientos, Isabel Fabregat, Snorri S Thorgeirsson, Aránzazu Sánchez

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 34 citations in OpenAlex.

  1. A Protocol for the Isolation of Oval Cells without Preconditioning.International journal of molecular sciences · 2024
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Cyclic Peptide-Based Biologics Regulating HGF-MET.International journal of molecular sciences · 2020
    Review
  7. Article
  8. Bone morphogenetic protein 9 as a key regulator of liver progenitor cells in DDC-induced cholestatic liver injury.Liver international : official journal of the International Association for the Study of the Liver · 2018
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. The Hippo-Salvador pathway restrains hepatic oval cell proliferation, liver size, and liver tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  18. Article
  19. Review
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

7 authors at 5 institutions in 3 countries.

Gaelle del CastilloDepartment Bioquímica y Biología Molecular II, Facultad de Farmacia, Universidad Complutense de Madrid, Plaza de Ramón y Cajal S/N, 28040-Madrid, Spain.
Valentina M Factor
Margarita Fernández
Alberto Alvarez-Barrientos
Isabel Fabregat
Snorri S Thorgeirsson
Aránzazu Sánchez
Universidad Complutense de Madrid · ESInstitut d'Investigació Biomédica de Bellvitge · ESNational Cancer Institute · USNational Institutes of Health · USSpanish National Centre for Cardiovascular Research · ES

Funding

The role of c-met in liver biologyZIABC010638 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI THORGEIRSSON, SNORRI · 2009 to 2013
$1.0M
The role of c-met in liver biologyZ01BC010638 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI THORGEIRSSON, SNORRI S · 2004 to 2008
$590k
6 · The paper itself

Abstract

The hepatocyte growth factor (HGF)/Met signaling system is essential for liver development, homeostasis, and function. In this study, we took advantage of a liver-specific, Met-conditional knockout mouse generated in our laboratory to address the molecular mechanisms of HGF/Met signaling in adult liver progenitor cell (oval cell) biology. For this purpose, we isolated oval cells from 3,5-diethoxycarbonyl-1,4-dihydro-collidine-treated Met(flx/flx) mice and established oval cell-derived cell lines that carried either functional (Met(flx/flx)) or a nonfunctional (Met(-/-)) met gene using virus-mediated Cre-loxP recombination. Oval cells lacking Met tyrosine kinase activity displayed neither Met phosphorylation nor activation of downstream targets and were refractory to HGF stimulation. Although Met(-/-) and Met(flx/flx) cells proliferated at similar rates under 10% serum, Met-deficient cells demonstrated decreased cell viability and were more prone to apoptosis when challenged with either serum starvation or the pro-apoptotic cytokine transforming growth factor-beta. Treatment with HGF reduced transforming growth factor-beta-mediated cell death in Met(flx/flx) but not Met(-/-) cells. Importantly, Met(flx/flx) and Met(-/-) cells both constitutively expressed hgf, and conditioned medium from serum-starved oval cells exhibited anti-apoptotic activity in Met(flx/flx) cells. Furthermore, serum-starved Met(flx/flx) cells showed persistent activation of the Met tyrosine kinase, suggesting HGF/Met autocrine regulation. In conclusion, these data reveal a critical, functional role for Met in oval cell survival through an autocrine mechanism.

Indexed as

AnimalsApoptosisCell SurvivalDicarbethoxydihydrocollidineHepatocyte Growth FactorHepatocytesIndicators and ReagentsMiceProto-Oncogene Proteins c-metSignal TransductionStem CellsTransforming Growth Factor betaDicarbethoxydihydrocollidineHepatocyte Growth FactorIndicators and ReagentsProto-Oncogene Proteins c-metTransforming Growth Factor beta

Identifiers

PMID18385520
PMCPMC2329833
OpenAlexW2020264462

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.