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Related Experiment Video

Updated: May 9, 2026

Isolation and Enrichment of Liver Progenitor Subsets Identified by a Novel Surface Marker Combination
08:52

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Published on: February 18, 2017

TWEAK induces liver progenitor cell proliferation.

Aniela Jakubowski1, Christine Ambrose, Michael Parr

  • 1Department of Exploratory Science, Biogen Idec Inc., Cambridge, Massachusetts 02142, USA. Aniela.Jakubowski@biogenidec.com

The Journal of Clinical Investigation
|August 20, 2005
PubMed
Summary
This summary is machine-generated.

Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) selectively stimulates liver oval cell proliferation via its receptor Fn14. This pathway is implicated in liver injury and regeneration, offering new therapeutic targets.

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Area of Science:

  • Hepatology
  • Cell Biology
  • Immunology

Background:

  • Progenitor (oval) cell expansion is a hallmark of liver injury when hepatocyte replication is impaired.
  • The precise mechanisms regulating oval cell proliferation remain largely unknown.
  • Oval cells are critical for liver regeneration, potentially differentiating into hepatocytes or biliary cells.

Purpose of the Study:

  • To investigate the role of TNF-like weak inducer of apoptosis (TWEAK) and its receptor Fn14 in regulating liver oval cell proliferation.
  • To determine if TWEAK selectively affects oval cells or mature hepatocytes.
  • To explore the potential involvement of the TWEAK/Fn14 pathway in human liver diseases.

Main Methods:

  • Utilized transgenic mice overexpressing TWEAK in hepatocytes.
  • Administered TWEAK-expressing adenovirus to wild-type and Fn14-null mice.
  • Induced liver injury using 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) in wild-type and Fn14-null mice.
  • Employed blocking anti-TWEAK monoclonal antibodies (mAbs).
  • Cultured and treated liver oval cells with TWEAK.
  • Analyzed Fn14 expression in human liver disease samples.

Main Results:

  • TWEAK administration led to periportal oval cell hyperplasia in wild-type mice, but not in Fn14-null mice.
  • Oval cell expansion induced by DDC was significantly reduced in Fn14-null mice and when TWEAK was blocked.
  • TWEAK demonstrated a selective mitogenic effect on cultured oval cells, with no impact on mature hepatocytes.
  • Fn14 expression was elevated in human chronic hepatitis C and other liver diseases compared to normal liver.

Conclusions:

  • TWEAK, acting through Fn14, selectively promotes liver oval cell proliferation.
  • The TWEAK/Fn14 pathway plays a significant role in liver regeneration and injury responses.
  • This pathway represents a potential therapeutic target for liver diseases characterized by impaired hepatocyte replication and oval cell expansion.