Evidence map›Paper›PMID 21898491›Full record

ArticleHepatology (Baltimore, Md.)2011

Tenascin-C: a novel mediator of hepatic ischemia and reperfusion injury.

Naohisa Kuriyama, Sergio Duarte, Takashi Hamada, Ronald W Busuttil, Ana J Coito

Open access · bronzeAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

29 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Tenascin-C in fibrosis in multiple organs: Translational implications.Seminars in cell & developmental biology · 2022
    Review
  7. Review
  8. Article
  9. Article
  10. Tenascin-C in Heart Diseases-The Role of Inflammation.International journal of molecular sciences · 2021
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Overproduction of Tenascin-C Driven by Lipid Accumulation in the Liver Aggravates Hepatic Ischemia/Reperfusion Injury in Steatotic Mice.Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society · 2019
    Article
  16. Internal Affairs: Tenascin-C as a Clinically Relevant, Endogenous Driver of Innate Immunity.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018
    Review
  17. Article
  18. Article
  19. Article
  20. Tenascins in Retinal and Optic Nerve Neurodegeneration.Frontiers in integrative neuroscience · 2017
    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

5 authors at 1 institution in 1 country.

Naohisa KuriyamaDumont-UCLA Transplant Center, Division of Liver and Pancreas Transplantation, Department of Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-7054, USA.
Sergio Duarte
Takashi Hamada
Ronald W Busuttil
Ana J Coito
University of California, Los Angeles · US

Funding

Matrix Metalloproteinases in Hepatic Ischemia and Reperfusion InjuryR01AI057832 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI COITO, ANA J. · 2004 to 2014
$3.5M
NIAID NIH HHS R01 AI057832NIAID NIH HHS R01AI057832
6 · The paper itself

Abstract

Hepatic ischemia/reperfusion (IRI) injury remains a major challenge in clinical orthotopic liver transplantation (OLT). Tenascin-C (Tnc) is an extracellular matrix protein (ECM) involved in various aspects of immunity and tissue injury. Using a Tnc-deficient mouse model, we present data that suggest an active role for Tnc in liver IRI. We show that Tnc-deficient mice have a reduction in liver damage and a significant improvement in liver regeneration after IRI. The inability of Tnc(-/-) mice to express Tnc significantly reduced the levels of active caspase-3/transferase-mediated dUTP nick end-labeling (TUNEL) apoptotic markers and enhanced the expression of the proliferation cell nuclear antigen (PCNA) after liver IRI. The lack of Tnc expression resulted in impaired leukocyte recruitment and decreased expressions of interleukin (IL)-1β, IL-6, and CXCL2 after liver reperfusion. Tnc-deficient livers were characterized by altered expression patterns of vascular adhesion molecules, such as vascular cell adhesion molecule-1 and platelet endothelial cell adhesion molecule-1 post-IRI. Moreover, matrix metalloproteinase-9 (MMP-9) synthesis, which facilitates leukocyte transmigration across vascular barriers in liver IRI, was markedly down-regulated in the absence of Tnc. We also show that Tnc is capable of inducing MMP-9 expression in isolated neutrophils through Toll-like receptor 4. Therefore, our data suggest that Tnc is a relevant mediator of the pathogenic events underlying liver IRI. The data also support the view that studies aimed at further understanding how newly synthesized ECM molecules, such as Tnc, participate in inflammatory responses are needed to improve therapeutic approaches in liver IRI.

Indexed as

AnimalsCaspase 3In Situ Nick-End LabelingIntercellular Adhesion Molecule-1Interleukin-1betaInterleukin-6LiverLiver RegenerationMatrix Metalloproteinase 9MicePlatelet Endothelial Cell Adhesion Molecule-1Reperfusion InjuryTenascinToll-Like Receptor 4Vascular Cell Adhesion Molecule-1Caspase 3Intercellular Adhesion Molecule-1Interleukin-1betaInterleukin-6Matrix Metalloproteinase 9Platelet Endothelial Cell Adhesion Molecule-1TenascinTlr4 protein, mouseToll-Like Receptor 4Vascular Cell Adhesion Molecule-1

Identifiers

PMID21898491
PMCPMC3230719
OpenAlexW2053081390

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.