Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Glucocorticoids decrease the bioavailability of TGF-beta which leads to a reduced TGF-beta signaling in hepatic

Ursula Bolkenius1, Daniela Hahn, Axel M Gressner

  • 1Institute of Clinical Chemistry and Pathobiochemistry, RWTH University Hospital Aachen, Pauwelsstr. 30, D-52074 Aachen, Germany.

Biochemical and Biophysical Research Communications
|November 24, 2004
PubMed
Summary

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

TGF-β1 and TGF-β2 family members differentially modulate tumor initiation and invasiveness of primary liver cancer in a MMP14-dependent manner.

Carcinogenesis·2026
Same author

Phosphatidylserine-Dependent Clearance of Damaged Red Blood Cells by Liver Sinusoidal Endothelial Cells in Alcohol-Related Liver Disease.

Biology·2026
Same author

Long-term Dynamic Virological Response Patterns and Clinical Outcomes in Hepatitis B Virus-related Cirrhosis: A Real-world 10-year Cohort Study.

Journal of clinical and translational hepatology·2026
Same author

Semi-automated isolation of parenchymal and non-parenchymal liver cells from mice and humans with enhanced stellate cell fraction.

Cell & bioscience·2026
Same author

Erratum: Follistatin-controlled activin-HNF4α-coagulation factor axis in liver progenitor cells determines outcome of acute liver failure.

Hepatology (Baltimore, Md.)·2025
Same author

Transforming Growth Factor-β Signaling in Alcohol-Associated Liver Disease: A Multicellular Perspective.

The American journal of pathology·2025

Glucocorticoids, like dexamethasone, reduce liver fibrosis by inhibiting transforming growth factor-beta (TGF-β) expression, secretion, and signaling in hepatic stellate cells (HSCs). This suggests a therapeutic target for liver disease.

Area of Science:

  • Molecular biology
  • Cell signaling
  • Hepatology

Background:

  • Glucocorticoids regulate physiological processes via transcription factors.
  • Transforming growth factor-beta (TGF-β) activates hepatic stellate cells (HSCs), promoting liver fibrosis.
  • Glucocorticoids may antagonize TGF-β signaling.

Purpose of the Study:

  • To investigate the influence of glucocorticoids on TGF-β and Smad expression, secretion, and signaling in activated HSCs.
  • To elucidate the molecular mechanisms of glucocorticoid action on TGF-β pathway.

Main Methods:

  • Gene-specific real-time PCR for mRNA expression analysis.
  • Enzyme-linked immunosorbent assay (ELISA) for TGF-β secretion.
  • Transfection techniques and reporter gene analysis for signaling pathway assessment.

Related Experiment Videos

Main Results:

  • Dexamethasone reduced TGF-β mRNA transcription and secretion in a time- and dose-dependent manner.
  • Reduced TGF-β secretion was restored by mifepristone.
  • Dexamethasone significantly down-regulated TGF-β-Smad signaling in primary HSCs and a HSC-related cell line (CFSC).

Conclusions:

  • Glucocorticoids inhibit TGF-β expression and secretion in activated HSCs.
  • Glucocorticoids lead to reduced TGF-β signaling, potentially mitigating liver fibrosis.
  • This study reveals a molecular mechanism for glucocorticoid antagonism of TGF-β in liver cells.