M2 macrophage-derived exosomal microRNA-411-5p impedes the activation of hepatic stellate cells by targeting CAMSAP1 in NASH model
Liver fibrosis is a severe stage of nonalcoholic fatty liver disease (NAFLD), which is closely associated with the activation of hepatic stellate cells (HSCs) and their interaction with macrophages. Exosomes can mediate crosstalk between macrophages and HSCs in NAFLD-associated fibrosis. We found th...
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| Published in | iScience Vol. 25; no. 7; p. 104597 |
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| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
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Elsevier Inc
15.07.2022
Elsevier |
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| Abstract | Liver fibrosis is a severe stage of nonalcoholic fatty liver disease (NAFLD), which is closely associated with the activation of hepatic stellate cells (HSCs) and their interaction with macrophages. Exosomes can mediate crosstalk between macrophages and HSCs in NAFLD-associated fibrosis. We found that M2 macrophage-derived exosomes significantly inhibit HSCs activation. RNA-seq studies revealed that miRNA-411-5p was decreased in serum exosomes of nonalcoholic steatohepatitis (NASH) patients as compared with that in healthy controls. Besides, miR-411-5p and M2 macrophage markers are decreased in the liver of the NASH model. We further proved that exosomal miR-411-5p from M2 macrophages inhibit HSCs activation and miR-411-5p directly downregulated the expression of Calmodulin-Regulated Spectrin-Associated Protein 1 (CAMSAP1) to inactivate stellate cells. Importantly, knockdown of CAMSAP1 also inhibited HSCs activation. This study contributes to understanding the underlying mechanism of HSCs activation and indicates CAMSAP1 may serve as a potential therapeutic target for NASH.
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•M2 macrophage markers are decreased in the HFHCD-induced rat model of NASH•M2 macrophage-derived exosomes inhibit HSCs activation via miR-411-5p•CAMSAP1 is a direct target of miR-411-5p•Knockdown of CAMSAP1 inhibits HSCs activation
Fibrosis; Biological sciences; Immunology |
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| AbstractList | Liver fibrosis is a severe stage of nonalcoholic fatty liver disease (NAFLD), which is closely associated with the activation of hepatic stellate cells (HSCs) and their interaction with macrophages. Exosomes can mediate crosstalk between macrophages and HSCs in NAFLD-associated fibrosis. We found that M2 macrophage-derived exosomes significantly inhibit HSCs activation. RNA-seq studies revealed that miRNA-411-5p was decreased in serum exosomes of nonalcoholic steatohepatitis (NASH) patients as compared with that in healthy controls. Besides, miR-411-5p and M2 macrophage markers are decreased in the liver of the NASH model. We further proved that exosomal miR-411-5p from M2 macrophages inhibit HSCs activation and miR-411-5p directly downregulated the expression of Calmodulin-Regulated Spectrin-Associated Protein 1 (CAMSAP1) to inactivate stellate cells. Importantly, knockdown of CAMSAP1 also inhibited HSCs activation. This study contributes to understanding the underlying mechanism of HSCs activation and indicates CAMSAP1 may serve as a potential therapeutic target for NASH. Liver fibrosis is a severe stage of nonalcoholic fatty liver disease (NAFLD), which is closely associated with the activation of hepatic stellate cells (HSCs) and their interaction with macrophages. Exosomes can mediate crosstalk between macrophages and HSCs in NAFLD-associated fibrosis. We found that M2 macrophage-derived exosomes significantly inhibit HSCs activation. RNA-seq studies revealed that miRNA-411-5p was decreased in serum exosomes of nonalcoholic steatohepatitis (NASH) patients as compared with that in healthy controls. Besides, miR-411-5p and M2 macrophage markers are decreased in the liver of the NASH model. We further proved that exosomal miR-411-5p from M2 macrophages inhibit HSCs activation and miR-411-5p directly downregulated the expression of Calmodulin-Regulated Spectrin-Associated Protein 1 ( CAMSAP1 ) to inactivate stellate cells. Importantly, knockdown of CAMSAP1 also inhibited HSCs activation. This study contributes to understanding the underlying mechanism of HSCs activation and indicates CAMSAP1 may serve as a potential therapeutic target for NASH. • M2 macrophage markers are decreased in the HFHCD-induced rat model of NASH • M2 macrophage-derived exosomes inhibit HSCs activation via miR-411-5p • CAMSAP1 is a direct target of miR-411-5p • Knockdown of CAMSAP1 inhibits HSCs activation Fibrosis; Biological sciences; Immunology Liver fibrosis is a severe stage of nonalcoholic fatty liver disease (NAFLD), which is closely associated with the activation of hepatic stellate cells (HSCs) and their interaction with macrophages. Exosomes can mediate crosstalk between macrophages and HSCs in NAFLD-associated fibrosis. We found that M2 macrophage-derived exosomes significantly inhibit HSCs activation. RNA-seq studies revealed that miRNA-411-5p was decreased in serum exosomes of nonalcoholic steatohepatitis (NASH) patients as compared with that in healthy controls. Besides, miR-411-5p and M2 macrophage markers are decreased in the liver of the NASH model. We further proved that exosomal miR-411-5p from M2 macrophages inhibit HSCs activation and miR-411-5p directly downregulated the expression of Calmodulin-Regulated Spectrin-Associated Protein 1 (CAMSAP1) to inactivate stellate cells. Importantly, knockdown of CAMSAP1 also inhibited HSCs activation. This study contributes to understanding the underlying mechanism of HSCs activation and indicates CAMSAP1 may serve as a potential therapeutic target for NASH.Liver fibrosis is a severe stage of nonalcoholic fatty liver disease (NAFLD), which is closely associated with the activation of hepatic stellate cells (HSCs) and their interaction with macrophages. Exosomes can mediate crosstalk between macrophages and HSCs in NAFLD-associated fibrosis. We found that M2 macrophage-derived exosomes significantly inhibit HSCs activation. RNA-seq studies revealed that miRNA-411-5p was decreased in serum exosomes of nonalcoholic steatohepatitis (NASH) patients as compared with that in healthy controls. Besides, miR-411-5p and M2 macrophage markers are decreased in the liver of the NASH model. We further proved that exosomal miR-411-5p from M2 macrophages inhibit HSCs activation and miR-411-5p directly downregulated the expression of Calmodulin-Regulated Spectrin-Associated Protein 1 (CAMSAP1) to inactivate stellate cells. Importantly, knockdown of CAMSAP1 also inhibited HSCs activation. This study contributes to understanding the underlying mechanism of HSCs activation and indicates CAMSAP1 may serve as a potential therapeutic target for NASH. Liver fibrosis is a severe stage of nonalcoholic fatty liver disease (NAFLD), which is closely associated with the activation of hepatic stellate cells (HSCs) and their interaction with macrophages. Exosomes can mediate crosstalk between macrophages and HSCs in NAFLD-associated fibrosis. We found that M2 macrophage-derived exosomes significantly inhibit HSCs activation. RNA-seq studies revealed that miRNA-411-5p was decreased in serum exosomes of nonalcoholic steatohepatitis (NASH) patients as compared with that in healthy controls. Besides, miR-411-5p and M2 macrophage markers are decreased in the liver of the NASH model. We further proved that exosomal miR-411-5p from M2 macrophages inhibit HSCs activation and miR-411-5p directly downregulated the expression of Calmodulin-Regulated Spectrin-Associated Protein 1 (CAMSAP1) to inactivate stellate cells. Importantly, knockdown of CAMSAP1 also inhibited HSCs activation. This study contributes to understanding the underlying mechanism of HSCs activation and indicates CAMSAP1 may serve as a potential therapeutic target for NASH. [Display omitted] •M2 macrophage markers are decreased in the HFHCD-induced rat model of NASH•M2 macrophage-derived exosomes inhibit HSCs activation via miR-411-5p•CAMSAP1 is a direct target of miR-411-5p•Knockdown of CAMSAP1 inhibits HSCs activation Fibrosis; Biological sciences; Immunology |
| ArticleNumber | 104597 |
| Author | Deng, Hong Wan, Zhiping Yu, Piaojian Sun, Yinfang Xu, Fen Yang, Xiaoan Liu, Xiaoquan |
| Author_xml | – sequence: 1 givenname: Zhiping surname: Wan fullname: Wan, Zhiping organization: Department of Infectious Diseases, the Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510630, China – sequence: 2 givenname: Xiaoan surname: Yang fullname: Yang, Xiaoan organization: Department of Infectious Diseases, the Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510630, China – sequence: 3 givenname: Xiaoquan surname: Liu fullname: Liu, Xiaoquan organization: Department of Infectious Diseases, the Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510630, China – sequence: 4 givenname: Yinfang surname: Sun fullname: Sun, Yinfang organization: Department of General Intensive Care Unit, the Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510630, China – sequence: 5 givenname: Piaojian surname: Yu fullname: Yu, Piaojian organization: Department of Endocrinology and Metabolism, the Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510630, China – sequence: 6 givenname: Fen surname: Xu fullname: Xu, Fen email: xufen3@mail.sysu.edu.cn organization: Department of Endocrinology and Metabolism, the Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510630, China – sequence: 7 givenname: Hong surname: Deng fullname: Deng, Hong email: dhong@mail.sysu.edu.cn organization: Department of Infectious Diseases, the Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510630, China |
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| Keywords | Biological sciences Immunology Fibrosis |
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