Evidence map›Paper›PMID 24349206›Full record

ArticlePloS one2013

The transcriptomic response of rat hepatic stellate cells to endotoxin: implications for hepatic inflammation and immune regulation.

Stephen A K Harvey, Anil Dangi, Ashish Tandon, Chandrashekhar R Gandhi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  8. Irisin Regulates the Functions of Hepatic Stellate Cells.Endocrinology and metabolism (Seoul, Korea) · 2020
    Article
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  10. Review
  11. Review
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  16. The lipoxin ANaunyn-Schmiedeberg's archives of pharmacology · 2017
    Article
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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 3 institutions in 1 country.

Stephen A K HarveyDepartment of Opthalmology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Anil DangiDepartment of Surgery, University of Cincinnati, Cincinnati, Ohio, United States of America ; Cincinnati VA Medical Center, Cincinnati, Ohio, United States of America.
Ashish TandonDepartment of Surgery, University of Cincinnati, Cincinnati, Ohio, United States of America.
Chandrashekhar R GandhiDepartment of Surgery, University of Cincinnati, Cincinnati, Ohio, United States of America ; Cincinnati VA Medical Center, Cincinnati, Ohio, United States of America ; Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, United States of America.
University of Cincinnati · USCincinnati Children's Hospital Medical Center · USUniversity of Pittsburgh · US

Funding

ROLE OF STELLATE CELLS IN LIVER FAILURER01DK054411 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GANDHI, CHANDRASHEKHAR R · 1998 to 2006
$1.7M
Mechanisms of Liver InjuryI01BX001174 · VA · VETERANS HEALTH ADMINISTRATION · PI GANDHI, CHANDRASHEKHAR R · 2012 to 2023
–
BLRD VA I01 BX001174NIDDK NIH HHS R01 DK054411NIDDK NIH HHS R01-DK54411PHS HHS P01A1081678
6 · The paper itself

Abstract

With their location in the perisinusoidal space of Disse, hepatic stellate cells (HSCs) communicate with all of the liver cell types both by physical association (cell body as well as cytosolic processes penetrating into sinusoids through the endothelial fenestrations) and by producing several cytokines and chemokines. Bacterial lipopolysaccharide (LPS), circulating levels of which are elevated in liver diseases and transplantation, stimulates HSCs to produce increased amounts of cytokines and chemokines. Although recent research provides strong evidence for the role of HSCs in hepatic inflammation and immune regulation, the number of HSC-elaborated inflammatory and immune regulatory molecules may be much greater then known at the present time. Here we report time-dependent changes in the gene expression profile of inflammatory and immune-regulatory molecules in LPS-stimulated rat HSCs, and their validation by biochemical analyses. LPS strongly up-regulated LPS-response elements (TLR2 and TLR7) but did not affect TLR4 and down-regulated TLR9. LPS also up-regulated genes in the MAPK, NFκB, STAT, SOCS, IRAK and interferon signaling pathways, numerous CC and CXC chemokines and IL17F. Interestingly, LPS modulated genes related to TGFβ and HSC activation in a manner that would limit their activation and fibrogenic activity. The data indicate that LPS-stimulated HSCs become a major cell type in regulating hepatic inflammatory and immunological responses by altering expression of numerous relevant genes, and thus play a prominent role in hepatic pathophysiology including liver diseases and transplantation.

Indexed as

AnimalsAntigen PresentationChemokinesDown-RegulationHepatic Stellate CellsInflammationLipopolysaccharidesLiverMaleMitogen-Activated Protein KinasesNF-kappa BRatsRats, Sprague-DawleyResponse ElementsRNA, MessengerSignal TransductionChemokinesLipopolysaccharidesMitogen-Activated Protein KinasesNF-kappa BRNA, MessengerToll-Like ReceptorsTransforming Growth Factor beta

Identifiers

PMID24349206
PMCPMC3857241
OpenAlexW2038280761

What OpenQuestion holds

Textmetadata
LicenceCC0
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.