2. Academic Validation
  3. Analysis of the Role of Stellate Cell VCAM-1 in NASH Models in Mice

Analysis of the Role of Stellate Cell VCAM-1 in NASH Models in Mice

  • Int J Mol Sci. 2023 Mar 2;24(5):4813. doi: 10.3390/ijms24054813.
Kyoung-Jin Chung 1,  Aigli-Ioanna Legaki 2,  Grigorios Papadopoulos 2,  Bettina Gercken 1,  Janine Gebler 1,  Robert F Schwabe 3,  Triantafyllos Chavakis 1,  Antonios Chatzigeorgiou 1 2
Affiliations

Affiliations

  • 1 Institute for Clinical Chemistry and Laboratory Medicine, University Hospital and Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, Fetscherstrasse 74, 01307 Dresden, Germany.
  • 2 Department of Physiology, Medical School, National and Kapodistrian University of Athens, 75 Mikras Asias Str., 11527 Athens, Greece.
  • 3 Department of Medicine, Columbia University, New York, NY 10032, USA.
PMID: 36902241 DOI: 10.3390/ijms24054813
Abstract

Non-alcoholic fatty liver disease (NAFLD) can progress to non-alcoholic steatohepatitis (NASH), characterized by inflammation and fibrosis. Fibrosis is mediated by hepatic stellate cells (HSC) and their differentiation into activated myofibroblasts; the latter process is also promoted by inflammation. Here we studied the role of the pro-inflammatory adhesion molecule vascular cell adhesion molecule-1 (VCAM-1) in HSCs in NASH. VCAM-1 expression was upregulated in the liver upon NASH induction, and VCAM-1 was found to be present on activated HSCs. We therefore utilized HSC-specific VCAM-1-deficient and appropriate control mice to explore the role of VCAM-1 on HSCs in NASH. However, HSC-specific VCAM-1-deficient mice, as compared to control mice, did not show a difference with regards to steatosis, inflammation and fibrosis in two different models of NASH. Hence, VCAM-1 on HSCs is dispensable for NASH development and progression in mice.

Keywords

hepatic stellate cells (HSCs); non-alcoholic fatty liver disease (NAFLD); non-alcoholic steatohepatitis (NASH); vascular cell adhesion molecule 1 (VCAM-1).

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