Evidence map›Paper›PMID 11896582›Full record

ArticleOncogene2002

Retinoic acid inhibits hepatic Jun N-terminal kinase-dependent signaling pathway in ethanol-fed rats.

Jayong Chung, Pollyanna R G Chavez, Robert M Russell, Xiang-Dong Wang

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 61 citations in OpenAlex.

  1. Retinoic acid signaling and metabolism in heart failure.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Journal of ginseng research · 2017
    Article
  8. Article
  9. Article
  10. Article
  11. Carotenoids and alcoholic liver disease.Hepatobiliary surgery and nutrition · 2013
    Article
  12. Pharmacological blockage of CYP2E1 and alcohol-mediated liver cancer: is the time ready?Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2013
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  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

4 authors at 2 institutions in 1 country.

Jayong ChungMolecular Carcinogenesis Section, Gastrointestinal Nutrition Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts, MA 02111, USA.
Pollyanna R G Chavez
Robert M Russell
Xiang-Dong Wang
Jean Mayer Human Nutrition Research Center on Aging · USTufts University · US

Funding

INTESTINAL METABOLISM OF BETA-CAROTENER01CA049195 · NCI · TUFTS UNIVERSITY BOSTON · PI RUSSELL, ROBERT M · 1991 to 2005
$1.2M
NCI NIH HHS R01CA49195
6 · The paper itself

Abstract

Retinoic acid (RA) supplementation suppresses ethanol-enhanced hepatocyte hyperproliferation in rats; however, little is known about the mechanism(s). Here, we investigated whether RA affects the protein kinase signaling pathways in the liver tissues of rats fed with a high dose of ethanol for a prolonged period of time (6 months). Results show that there were greater levels of phosphorylated Jun N-terminal kinase (JNK) and phosphorylated c-Jun protein, but not total JNK protein, in livers of ethanol-fed rats vs those of controls. Moreover, ethanol feeding to rats increased the levels of phosphorylated mitogen-activated protein kinase kinase-4 (MKK-4) and decreased the levels of mitogen-activated kinase phosphatase-1 (MKP-1) in liver tissue. However, hepatic levels of phosphorylated-p38 protein and total-p38 protein were not altered by the ethanol treatment. In contrast, all-trans-RA supplementation at two doses in ethanol-fed rats greatly attenuated the ethanol-induced hepatic phosphorylation of MKK-4, phosphorylated-JNK and c-Jun proteins. The level of MKP-1 was increased in ethanol-fed rats supplemented with all-trans-RA. Further, ethanol-induced hepatocyte hyperproliferation, measured by immunostaining for proliferating cell nuclear antigen, were markedly decreased by all-trans-RA supplementation. Interestingly, hepatic apoptosis in the liver of ethanol-fed rats after 6 months of treatment decreased significantly. This decrease of hepatic apoptosis in ethanol-fed rats was prevented by all-trans-RA supplementation in a dose-dependent manner. The results from these studies indicate that restoration of RA homeostasis is critical for the regulation of JNK-dependent signaling pathway and apoptosis in the liver of ethanol-fed rats.

Indexed as

Cell Cycle ProteinsMAP Kinase Signaling SystemPhosphoprotein PhosphatasesAnimalsApoptosisCell DivisionDual Specificity Phosphatase 1EthanolImmediate-Early ProteinsImmunohistochemistryJNK Mitogen-Activated Protein KinasesLiverMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPhosphorylationCell Cycle ProteinsDual Specificity Phosphatase 1Dusp1 protein, ratEthanolImmediate-Early ProteinsJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase KinasesMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPhosphoprotein PhosphatasesProliferating Cell Nuclear AntigenProtein Phosphatase 1Protein Tyrosine PhosphatasesProto-Oncogene Proteins c-junTretinoin

Identifiers

PMID11896582
OpenAlexW2078889074

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.