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

Research output: Contribution to journal › Research article › Contributed › peer-review

Contributors

  • Kyoung Jin Chung - , Institute of Clinical Chemistry and Laboratory Medicine, University Hospital Carl Gustav Carus Dresden (Author)
  • Aigli Ioanna Legaki - , National and Kapodistrian University of Athens (Author)
  • Grigorios Papadopoulos - , National and Kapodistrian University of Athens (Author)
  • Bettina Gercken - , TUD Dresden University of Technology, Institute for Clinical Chemistry and Laboratory Medicine (Author)
  • Janine Gebler - , TUD Dresden University of Technology, Institute for Clinical Chemistry and Laboratory Medicine (Author)
  • Robert F. Schwabe - , Columbia University (Author)
  • Triantafyllos Chavakis - , Institute of Clinical Chemistry and Laboratory Medicine, University Medicine (Faculty of Medicine and University Hospital) (Joint last author)
  • Antonios Chatzigeorgiou - , National and Kapodistrian University of Athens, Institute for Clinical Chemistry and Laboratory Medicine, Medical Faculty Carl Gustav Carus (Joint last author)

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.

Details

Original languageEnglish
Article number4813
Number of pages12
JournalInternational journal of molecular sciences
Volume24
Issue number5
Publication statusPublished - 2 Mar 2023
Peer-reviewedYes

External IDs

PubMed 36902241
WOS 000947621900001

Keywords

ASJC Scopus subject areas

Keywords

  • hepatic stellate cells (HSCs), non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), vascular cell adhesion molecule 1 (VCAM-1), Liver Cirrhosis/metabolism, Mice, Inbred C57BL, Inflammation/metabolism, Hepatic Stellate Cells/metabolism, Non-alcoholic Fatty Liver Disease/metabolism, Animals, Liver/metabolism, Mice, Vascular Cell Adhesion Molecule-1/metabolism, Disease Models, Animal

Library keywords