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.
|Fachzeitschrift||International journal of molecular sciences|
|Publikationsstatus||Veröffentlicht - 2 März 2023|
ASJC Scopus Sachgebiete
- 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