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Filamin A is overexpressed in non-alcoholic steatohepatitis and contributes to the progression of inflammation and fibrosis

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机构： [1]State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, 610041, China [2]Molecular Toxicology Laboratory of Sichuan Provincial Education Office, Institute of Systems Epidermiology, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, 610041, China [3]Department of Pathology, Mianyang Central Hospital, School of Medicine, University of Electronic Science and Technology of China, Mianyang, 621000, China [4]Department of Clinical Laboratory, Mianyang Central Hospital, School of Medicine, University of Electronic Science and Technology of China, Mianyang, 621000, China

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Non-alcoholic steatohepatitis (NASH) is a chronic and progressive liver disease characterized by steatosis, inflammation, and fibrosis. Filamin A (FLNA), an actin-binding protein, is involved in various cell functions, including the regulation of immune cells and fibroblasts. However, its role in the development of NASH through inflammation and fibrogenesis is not fully understood. In this study, we found that FLNA expression was increased in liver tissues of patients with cirrhosis and mice with non-alcoholic fatty liver disease (NAFLD)/NASH and fibrosis. Immunofluorescence analysis showed that FLNA was primarily expressed in macrophages and hepatic stellate cells (HSCs). Knocking down of FLNA by specific shRNA in phorbol-12-myristate-13-acetate (PMA)-derived THP-1 macrophages reduced lipopolysaccharide (LPS)-stimulated inflammatory response. The decreased mRNA levels of inflammatory cytokines and chemokines and suppression of the STAT3 signaling were observed in FLNA-downregulated macrophages. In addition, knockdown of FLNA in immortalized human hepatic stellate cells (LX-2 cells) resulted in decreased mRNA levels of fibrotic cytokines and enzymes involved in collagen synthesis, as well as increased levels of metalloproteinases and pro-apoptotic proteins. Overall, these results suggest that FLNA may contribute to the pathogenesis of NASH through its role in the regulation of inflammatory and fibrotic mediators.Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.

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出版当年[2023]版：

大类 | 3 区生物学

小类 | 3 区生物物理 4 区生化与分子生物学

最新[2023]版：

大类 | 3 区生物学

小类 | 3 区生物物理 4 区生化与分子生物学

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第一作者机构： [1]State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, 610041, China

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通讯作者：

通讯机构： [1]State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, 610041, China [2]Molecular Toxicology Laboratory of Sichuan Provincial Education Office, Institute of Systems Epidermiology, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, 610041, China [*1]Molecular Toxicology Laboratory of Sichuan Provincial Education office, Institute of Systems Epidemiology, West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, Sichuan, 610041, China. [*2]State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan, 610041, China.

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