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
  • 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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