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Related Experiment Video

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3D Imaging of the Liver Extracellular Matrix in a Mouse Model of Non-Alcoholic Steatohepatitis
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A Microphysiological System for Studying Nonalcoholic Steatohepatitis.

Tomasz Kostrzewski1, Paloma Maraver1, Larissa Ouro-Gnao1

  • 1CN Bio Innovations Ltd. Welwyn Garden City Hertfordshire United Kingdom.

Hepatology Communications
|January 8, 2020
PubMed
Summary
This summary is machine-generated.

A new human in vitro model using microphysiological systems accurately mimics nonalcoholic steatohepatitis (NASH) and its associated inflammation and fibrosis. This advanced NASH model, incorporating PNPLA3 mutations, aids in understanding disease mechanisms and testing therapeutics.

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Area of Science:

  • Hepatology
  • Translational Medicine
  • Biotechnology

Background:

  • Nonalcoholic steatohepatitis (NASH) is a severe form of nonalcoholic fatty liver disease (NAFLD) lacking approved treatments.
  • Current preclinical models inadequately represent human NASH complexity.
  • Understanding genetic and molecular pathways in NASH is crucial.

Purpose of the Study:

  • To develop a human in vitro co-culture NASH model using a microphysiological system (MPS).
  • To investigate the role of PNPLA3 mutations in NASH pathogenesis within this model.
  • To assess the model's utility for studying NASH mechanisms and evaluating potential therapies.

Main Methods:

  • Primary human hepatocytes, Kupffer cells, and hepatic stellate cells were co-cultured as microtissues in a 3D perfused MPS.
  • Microtissues were exposed to free fatty acids for two weeks to induce a NASH-like phenotype.
  • PNPLA3 I148M mutant and wild-type hepatic stellate cells were utilized to assess mutation impact.

Main Results:

  • The MPS co-culture model successfully replicated key NASH features: hepatic fat accumulation, inflammation, and profibrotic marker expression.
  • Lipopolysaccharide addition amplified the pro-inflammatory response.
  • Obeticholic acid demonstrated amelioration of the NASH phenotype in the model.
  • PNPLA3 I148M mutant stellate cells exacerbated the NASH phenotype and promoted a more pro-inflammatory milieu.

Conclusions:

  • The developed MPS model accurately recapitulates advanced NAFLD/NASH phenotypes, offering a valuable tool for disease mechanism exploration.
  • The PNPLA3 I148M mutation in hepatic stellate cells significantly enhances the NASH disease phenotype and inflammation in this co-culture system.
  • This model provides a platform for advancing research into NASH pathogenesis and therapeutic development.