Evidence map›Paper›PMID 16083721›Full record

ArticleGastroenterology2005

Cholangiocyte endothelin 1 and transforming growth factor beta1 production in rat experimental hepatopulmonary syndrome.

Bao Luo, Liping Tang, Zhishan Wang, Junlan Zhang, Yiqun Ling, Wenguang Feng, Ju-Zhong Sun, Cecil R Stockard, Andra R Frost, Yiu-Fai Chen and 2 more

Abstract readComparative Study
In one paragraph

Article in Gastroenterology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 79 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Hepatopulmonary syndrome.JHEP reports : innovation in hepatology · 2022
    Review
  6. Cellular crosstalk during liver regeneration: unity in diversity.Cell communication and signaling : CCS · 2022
    Review
  7. Article
  8. The TGFβ1 Receptor Antagonist GW788388 Reduces JNK Activation and Protects Against Acetaminophen Hepatotoxicity in Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2019
    Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Hepatopulmonary Syndrome.Digestive diseases and sciences · 2015
    Review
  16. Review
  17. Article
  18. The relationship between hepatopulmonary syndrome and altitude.Canadian journal of gastroenterology & hepatology · 2014
    Article
  19. Article
  20. Advances in cholangiocyte immunobiology.American journal of physiology. Gastrointestinal and liver physiology · 2012
    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

12 authors at 1 institution in 1 country.

Bao LuoDepartment of Internal Medicine and Liver Center, University of Alabama at Birmingham, 35294, USA.
Liping Tang
Zhishan Wang
Junlan Zhang
Yiqun Ling
Wenguang Feng
Ju-Zhong Sun
Cecil R Stockard
Andra R Frost
Yiu-Fai Chen
William E Grizzle
Michael B Fallon
University of Alabama at Birmingham · US

Funding

MEDIATORS OF PULMONARY VASODILATATION IN LIVER DISEASER01DK056804 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI FALLON, MICHAEL B · 2000 to 2013
$3.6M
TIGHT JUNCTION IN CHOLESTASIS--A MOLECULAR APPROACHK11DK002030 · NIDDK · YALE UNIVERSITY · PI FALLON, MICHAEL B · 1991 to 1995
–
NIDDK NIH HHS DK02030NIDDK NIH HHS R01 DK056804
6 · The paper itself

Abstract

BACKGROUND &

aimsHepatic production and release of endothelin 1 plays a central role in experimental hepatopulmonary syndrome after common bile duct ligation by stimulating pulmonary endothelial nitric oxide production. In thioacetamide-induced nonbiliary cirrhosis, hepatic endothelin 1 production and release do not occur, and hepatopulmonary syndrome does not develop. However, the source and regulation of hepatic endothelin 1 after common bile duct ligation are not fully characterized. We evaluated the sources of hepatic endothelin 1 production after common bile duct ligation in relation to thioacetamide cirrhosis and assessed whether transforming growth factor beta1 regulates endothelin 1 production.

methodsHepatopulmonary syndrome and hepatic and plasma endothelin 1 levels were evaluated after common bile duct ligation or thioacetamide administration. Cellular sources of endothelin 1 were assessed by immunohistochemistry and laser capture microdissection of cholangiocytes. Transforming growth factor beta1 expression and signaling were assessed by using immunohistochemistry and Western blotting and by evaluating normal rat cholangiocytes.

resultsHepatic and plasma endothelin 1 levels increased and hepatopulmonary syndrome developed only after common bile duct ligation. Hepatic endothelin 1 and transforming growth factor beta1 levels increased over a similar time frame, and cholangiocytes were a major source of each peptide. Transforming growth factor beta1 signaling in cholangiocytes in vivo was evident by increased phosphorylation and nuclear localization of Smad2, and hepatic endothelin 1 levels correlated directly with liver transforming growth factor beta1 and phosphorylated Smad2 levels. Transforming growth factor beta1 also stimulated endothelin 1 promoter activity, expression, and production in normal rat cholangiocytes.

conclusionsCholangiocytes are a major source of hepatic endothelin 1 production during the development of hepatopulmonary syndrome after common bile duct ligation, but not in thioacetamide-induced cirrhosis. Transforming growth factor beta1 stimulates cholangiocyte endothelin 1 expression and production. Cholangiocyte-derived endothelin 1 may be an important endocrine mediator of experimental hepatopulmonary syndrome.

Indexed as

AnimalsBase SequenceBiomarkersBiopsy, NeedleBlood Gas AnalysisBlotting, NorthernBlotting, WesternCells, CulturedDisease Models, AnimalEndothelin-1Hepatopulmonary SyndromeImmunohistochemistryLiver Function TestsMaleMolecular Sequence DataProbabilityBiomarkersEndothelin-1Tgfb1 protein, ratTransforming Growth Factor betaTransforming Growth Factor beta1

Identifiers

PMID16083721
PMCPMC2830806
OpenAlexW2047306058

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.