Evidence map›Paper›PMID 22318920›Full record

ArticleHepatology (Baltimore, Md.)2012

Fibronectin is essential for survival but is dispensable for proliferation of hepatocytes in acute liver injury in mice.

Kei Moriya, Keiko Sakai, Michel H Yan, Takao Sakai

Open access · greenAbstract readComparative Study
In one paragraph

Article in Hepatology (Baltimore, Md.), 2012. 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
1.3field-weighted citation impact, top 20% 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, 32 citations in OpenAlex.

  1. Article
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  5. Fibronectin has multifunctional roles in posterior capsular opacification (PCO).Matrix biology : journal of the International Society for Matrix Biology · 2020
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  11. ER stress-mediated cell damage contributes to the release of EDAJournal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2017
    Article
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  13. Salvianolate Protects Hepatocytes from Oxidative Stress by Attenuating Mitochondrial Injury.Evidence-based complementary and alternative medicine : eCAM · 2016
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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

4 authors at 2 institutions in 1 country.

Kei MoriyaDepartment of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA.
Keiko Sakai
Michel H Yan
Takao Sakai
Cerner (United States) · USCenter for Rheumatology · US

Funding

Fibronectin deposition and TGF-beta activation in liver fibrosisR01DK074538 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI SAKAI, TAKAO · 2007 to 2011
$1.5M
NIDDK NIH HHS DK074538NIDDK NIH HHS R01 DK074538
6 · The paper itself

Abstract

unlabelledAcute liver injury causes massive hepatocyte apoptosis and/or fatal liver damage. Fibronectin, an extracellular matrix glycoprotein, is prominently expressed during adult tissue repair. However, the extent of fibronectin dependence on hepatocyte response to acute liver damage remains to be defined. Because identification of hepatic survival factors is critical for successful therapeutic intervention in liver failure, this relationship has been investigated using a fibronectin-deficient mouse model of acute liver injury. Here, we show that lack of fibronectin induces significantly increased hepatocyte apoptosis, which is accompanied by significant down-regulation of the antiapoptotic protein, B-cell lymphoma-extra large (Bcl-xL). Furthermore, fibronectin deficiency leads to a significantly elevated production of hepatocyte growth factor in hepatic stellate cells postinjury, which, in turn, results in an earlier onset and acceleration of hepatocyte regeneration. Primary hepatocytes on fibronectin are protected from reactive oxygen species-induced cellular damage, retaining the expression of Bcl-xL, whereas those on type I collagen are not. This retained expression of Bcl-xL is inhibited by the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002.

conclusionWe provide evidence that fibronectin-mediated matrix survival signals for hepatocytes are transduced through the PI3K/Bcl-xL-signaling axis in response to injury. This work defines fibronectin as a novel antiapoptotic factor for hepatocytes after acute liver injury, but demonstrates that fibronectin is not essential for subsequent hepatocyte proliferation.

Indexed as

AnimalsBlotting, WesternCell ProliferationCells, CulturedCell SurvivalChemical and Drug Induced Liver InjuryDisease Models, AnimalDown-RegulationEnzyme-Linked Immunosorbent AssayFemaleFibronectinsFluorescent Antibody TechniqueGene Expression RegulationHepatocyte Growth FactorHepatocytesImmunohistochemistryFibronectinsHepatocyte Growth Factor

Identifiers

PMID22318920
PMCPMC3355232
OpenAlexW2033121381

What OpenQuestion holds

Textmetadata
LicenceTDM
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.