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Mapping Hepatic Stellate Cell Morphology in Mouse Models of Liver Fibrosis
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Rat liver myofibroblasts and hepatic stellate cells differ in CD95-mediated apoptosis and response to TNF-alpha

Bernhard Saile1, Nina Matthes, Katrin Neubauer

  • 1Department of Internal Medicine, Section of Gastroenterology and Endocrinology, University of Göttingen, Germany.

American Journal of Physiology. Gastrointestinal and Liver Physiology
|July 18, 2002
PubMed

Insights

Rat liver myofibroblasts (rMF) and activated hepatic stellate cells (HSC) differ significantly. rMF show less apoptosis and distinct CD95 system responses, indicating they are separate cell populations with fibrogenic potential.

Area of Science:

  • Cell Biology
  • Hepatology
  • Fibrosis Research

Background:

  • Activated hepatic stellate cells (HSC) are primary matrix producers in liver disease.
  • Rat liver myofibroblasts (rMF) also possess fibrogenic potential.
  • Differences in lifespan and apoptosis exist between activated HSC and rMF in culture.

Purpose of the Study:

  • To investigate and compare the characteristics of activated HSC and rMF.
  • To elucidate the role of the CD95 system in the apoptosis of these cell types.
  • To determine the differential responses of activated HSC and rMF to apoptosis-inducing stimuli.

Main Methods:

  • Cell culture of activated HSC and rMF.
  • Assessment of spontaneous apoptosis rates.
  • Quantification of CD95 receptor (CD95R) and ligand (CD95L) expression.
  • Induction of apoptosis using agonistic antibodies against CD95.
  • Evaluation of apoptosis in response to transforming growth factor-beta and tumor necrosis factor-alpha (TNF-alpha).

Main Results:

  • rMF exhibited minimal spontaneous apoptosis, while activated HSC showed significant apoptosis (18%).
  • rMF expressed 70% more CD95R than activated HSC; CD95L was detected only in activated HSC.
  • CD95 system stimulation induced rapid apoptosis in rMF (2h) but slower apoptosis in activated HSC (5.3h, 40%).
  • Transforming growth factor-beta reduced apoptosis in both cell types.
  • Tumor necrosis factor-alpha upregulated apoptosis specifically in rMF.

Conclusions:

  • Activated HSC and rMF represent distinct cell populations.
  • Differential expression of CD95 components and varied responses to TNF-alpha support their classification as separate cell types.
  • These findings have implications for understanding liver fibrogenesis and therapeutic targeting.

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