Evidence map›Paper›PMID 24493010›Full record

ArticleHepatology (Baltimore, Md.)2014

Plasmacytoid dendritic cell-derived IFN-α promotes murine liver ischemia/reperfusion injury by induction of hepatocyte IRF-1.

Antonino Castellaneta, Osamu Yoshida, Shoko Kimura, Shinichiro Yokota, David A Geller, Noriko Murase, Angus W Thomson

Open access · bronzeAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.7field-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

32 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
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  4. The Role of Interferon Regulatory Factors in Liver Diseases.International journal of molecular sciences · 2024
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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

7 authors at 1 institution in 1 country.

Antonino CastellanetaThomas E. Starzl Transplantation Institute, Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Osamu Yoshida
Shoko Kimura
Shinichiro Yokota
David A Geller
Noriko Murase
Angus W Thomson
University of Pittsburgh · US

Funding

University of Pittsburgh Clinical and Translational Science InstituteUL1TR000005 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$50.8M
Interdisciplinary Training in Transplantation BiologyT32AI074490 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Angus W Thomson · 2007 to 2026
$4.2M
Liver Antigen - Presenting Cells in Hepatic Injury and TransplantationP01AI081678 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI THOMSON, ANGUS W · 2009 to 2010
$2.8M
NCATS NIH HHS UL1 TR000005NIAID NIH HHS NIH T32 AI74490NIAID NIH HHS P01 AI081678NIAID NIH HHS P01 AI81678NIAID NIH HHS T32 AI074490
6 · The paper itself

Abstract

unlabelledPlasmacytoid dendritic cells (pDC) constitute the body's principal source of type I interferon (IFN) and are comparatively abundant in the liver. Among various cytokines implicated in liver ischemia and reperfusion (I/R) injury, type I IFNs have been described recently as playing an essential role in its pathogenesis. Moreover, type I IFNs have been shown to up-regulate hepatocyte expression of IFN regulatory factor 1 (IRF-1), a key transcription factor that regulates apoptosis and induces liver damage after I/R. Our aim was to ascertain the capacity of IFN-α released by liver pDC to induce liver damage through hepatic IRF-1 up-regulation after I/R injury. Our findings show that liver pDC mature and produce IFN-α in response to liver I/R. Liver pDC isolated after I/R induced elevated levels of IRF-1 production by hepatocytes compared with liver pDC isolated from sham-operated mice. Notably, hepatic IRF-1 expression was reduced significantly by neutralizing IFN-α. In vivo, IFN-α neutralization protected the liver from I/R injury by reducing hepatocyte apoptosis. This was associated with impaired expression of IRF-1 and proapoptotic molecules such as Fas ligand, its receptor (Fas) and death receptor 5, which are regulated by IRF-1. Furthermore, pDC-depleted mice failed to up-regulate hepatic IFN-α and displayed less liver injury associated with reduced levels of hepatic interleukin (IL)-6, tumor necrosis factor-α, and hepatocyte apoptosis after I/R compared with controls.

conclusionthese data support the hypothesis that IFN-α derived from liver pDC plays a key role in the pathogenesis of liver I/R injury by enhancing apoptosis as a consequence of induction of hepatocyte IRF-1 expression.

Indexed as

AnimalsApoptosisCells, CulturedDendritic CellsDisease Models, AnimalHepatocytesInterferon-alphaInterferon Regulatory Factor-1Interleukin-6Liver DiseasesMaleMiceMice, Inbred C57BLMice, KnockoutReperfusion InjuryTumor Necrosis Factor-alphaInterferon-alphaInterferon Regulatory Factor-1Interleukin-6interleukin-6, mouseIRF1 protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID24493010
PMCPMC4077928
OpenAlexW1791175067

What OpenQuestion holds

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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.