Evidence map›Paper›PMID 20722001›Full record

ArticleHepatology (Baltimore, Md.)2010

Liver-specific β-catenin knockout mice have bile canalicular abnormalities, bile secretory defect, and intrahepatic cholestasis.

Tzu-Hsuan Yeh, Lindsay Krauland, Vijay Singh, Baobo Zou, Prathab Devaraj, Donna B Stolz, Jonathan Franks, Satdarshan P S Monga, Eizaburo Sasatomi, Jaideep Behari

Open access · greenAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

42 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Wnt/β-Catenin Signaling in Liver Pathobiology.Annual review of pathology · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. β-Catenin Signaling Regulates theJournal of virology · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Neuroprotective Activity of Methanolic Extract ofEvidence-based complementary and alternative medicine : eCAM · 2020
    Article
  17. Article
  18. Article
  19. Review
  20. Article
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

10 authors at 1 institution in 1 country.

Tzu-Hsuan YehDepartment of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, PA 15213, USA.
Lindsay Krauland
Vijay Singh
Baobo Zou
Prathab Devaraj
Donna B Stolz
Jonathan Franks
Satdarshan P S Monga
Eizaburo Sasatomi
Jaideep Behari
University of Pittsburgh · US

Funding

Role of Beta-Catenin in the Molecular Pathogenesis of Alcoholic SteatohepatitisK08AA017622 · NIAAA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BEHARI, JAIDEEP · 2008 to 2012
$1.0M
NIAAA NIH HHS 1K08AA017622-01NIAAA NIH HHS K08 AA017622
6 · The paper itself

Abstract

unlabelledBeta-catenin plays important roles in liver physiology and hepatocarcinogenesis. While studying the role of β-catenin in diet-induced steatohepatitis, we recently found that liver-specific β-catenin knockout (KO) mice exhibit intrahepatic cholestasis. This study was undertaken to further characterize the role of β-catenin in biliary physiology. KO mice and wild-type (WT) littermates were fed standard chow or a diet supplemented with 0.5% cholic acid for 2 weeks. Chow-fed KO mice had higher serum and hepatic total bile acid levels and lower bile flow rate than WT mice. Expression levels of bile acid biosynthetic genes were lower and levels of major bile acid exporters were similar, which therefore could not explain the KO phenotype. Despite loss of the tight junction protein claudin-2, KO mice had preserved functional integrity of tight junctions. KO mice had bile canalicular morphologic abnormalities as evidenced by staining for F-actin and zona occludens 1. Electron microscopy revealed dilated and tortuous bile canaliculi in KO livers along with decreased canalicular and sinusoidal microvilli. KO mice on a cholic acid diet had higher hepatic and serum bile acid levels, bile ductular reaction, increased pericellular fibrosis, and dilated, misshapen bile canaliculi. Compensatory changes in expression levels of several bile acid transporters and regulatory genes were found in KO livers.

conclusionLiver-specific loss of β-catenin leads to defective bile canalicular morphology, bile secretory defect, and intrahepatic cholestasis. Thus, our results establish a critical role for β-catenin in biliary physiology.

Indexed as

Animalsbeta CateninBileBile Acids and SaltsBile CanaliculiCholestasis, IntrahepaticCholic AcidDietFemaleLiverMiceMice, Inbred C57BLMice, Knockoutbeta CateninBile Acids and SaltsCholic Acid

Identifiers

PMID20722001
PMCPMC2947599
OpenAlexW2010818022

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.