| Literature DB >> 34523053 |
Shogo Kawaguchi1, Hirotake Sakuraba2, Momone Horiuchi3, Jiangli Ding3, Tomoh Matsumiya3, Kazuhiko Seya3, Chikara Iino2, Tetsu Endo2, Hidezumi Kikuchi2, Shukuko Yoshida2,4, Hiroto Hiraga2, Shinsaku Fukuda2, Tadaatsu Imaizumi3.
Abstract
The activation of innate immune system is essential for the pathogenesis of nonalcoholic steatohepatitis (NASH). Among pattern recognition receptors, it is well-characterized that toll-like receptors (TLRs) are deeply involved in the development of NASH to reflect exposure of the liver to gut-driven endotoxins. In contrast, it has not been elucidated whether retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs) are similarly implicated in the disease progression. In the present study, we examined the expression of melanoma differentiation-associated antigen 5 (MDA5), known to be a member of RLRs, in a diet-induced murine model of NASH. The liver tissues were collected from C57BL/6 J mice at 1, 3, and 6 weeks after choline-deficient L-amino acid-defined high-fat diet (CDAHFD), and the expression of MDA5 was analyzed by western blotting, immunofluorescence (IF), and real-time quantitative PCR (qPCR). The results of western blotting showed that hepatic expression of MDA5 was increased at 3 and 6 weeks. In IF, MDA5-positive cells co-expressed F4/80 and CD11b, indicating they were activated macrophages, and these cells began to appear at 1 week after CDAHFD. The mRNA expression of MDA5 was significantly upregulated at 1 week. Additionally, we performed IF using liver biopsy specimens collected from 11 patients with nonalcoholic fatty liver diseases (NAFLD), and found that MDA5-positive macrophages were detected in eight out of eleven patients. In an in vitro study, MDA5 was induced upon stimulation with lipopolysaccharide in murine bone marrow-derived macrophages and THP-1 cells. Our findings suggest that MDA5 may be involved in the inflammation of NASH.Entities:
Keywords: CD11b; CDAHFD.; F4/80; MDA5; Macrophage; NASH
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Year: 2021 PMID: 34523053 DOI: 10.1007/s10753-021-01550-8
Source DB: PubMed Journal: Inflammation ISSN: 0360-3997 Impact factor: 4.092