Institute for Clinical Chemistry and Laboratory Medicine, University Hospital and Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, Fetscherstrasse 74, 01307 Dresden, Germany.
Department of Physiology, Medical School, National and Kapodistrian University of Athens, 75 Mikras Asias Str., 11527 Athens, Greece.
Int J Mol Sci. 2023 Mar 2;24(5):4813. doi: 10.3390/ijms24054813.
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.
非酒精性脂肪性肝病 (NAFLD) 可进展为非酒精性脂肪性肝炎 (NASH)，其特征为炎症和纤维化。纤维化由肝星状细胞 (HSC) 及其向活化肌成纤维细胞的分化介导；炎症也促进了这一过程。在此，我们研究了促炎黏附分子血管细胞黏附分子-1 (VCAM-1) 在 NASH 中 HSCs 中的作用。NASH 诱导时，肝脏中 VCAM-1 的表达上调，并且在活化的 HSCs 中发现了 VCAM-1。因此，我们利用 HSC 特异性 VCAM-1 缺陷和适当的对照小鼠来探索 VCAM-1 在 NASH 中对 HSCs 的作用。然而，与对照组小鼠相比，HSC 特异性 VCAM-1 缺陷小鼠在两种不同的 NASH 模型中，在脂肪变性、炎症和纤维化方面没有差异。因此，HSCs 上的 VCAM-1 对于 NASH 在小鼠中的发生和进展不是必需的。
