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Tytuł pozycji:

The S100 calcium-binding protein A11 promotes hepatic steatosis through RAGE-mediated AKT-mTOR signaling.

Tytuł :
The S100 calcium-binding protein A11 promotes hepatic steatosis through RAGE-mediated AKT-mTOR signaling.
Autorzy :
Teng F; Department of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Guangzhou, China.
Jiang J; The Key Laboratory of Metabolism and Molecular Medicine, the Ministry of Education, Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China.
Zhang J; Key Laboratory of Functional and Clinical Translational Medicine, Department of General Medicine, Xiamen Medical College, Xiamen, China.
Yuan Y; Department of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Guangzhou, China.
Li K; Department of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Guangzhou, China.
Zhou B; The Key Laboratory of Metabolism and Molecular Medicine, the Ministry of Education, Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China.
Zhou X; The First Affiliated Hospital of Xiamen University, Xiamen, China.
Liu W; Department of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Guangzhou, China.
Zhang P; Department of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Guangzhou, China.
Liu D; Department of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Guangzhou, China.
Zheng M; MAFLD Research Center, Department of Hepatology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China; Key Laboratory of Diagnosis and Treatment for The Development of Chronic Liver Disease, Zhejiang Province, Wenzhou, Zhejiang, China.
Lu Y; The Key Laboratory of Metabolism and Molecular Medicine, the Ministry of Education, Department of Endocrinology and Metabolism, Zhongshan Hospital, Fudan University, Shanghai, China. Electronic address: .
Zhang H; Department of Endocrinology and Metabolism, Nanfang Hospital, Southern Medical University, Guangzhou, China; Guangdong Provincial Key Laboratory of Shock and Microcirculation, Guangzhou, China. Electronic address: .
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Źródło :
Metabolism: clinical and experimental [Metabolism] 2021 Apr; Vol. 117, pp. 154725. Date of Electronic Publication: 2021 Feb 09.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
Język :
English
Imprint Name(s) :
Publication: Philadelphia, PA : W.B. Saunders
Original Publication: New York, Grune & Stratton.
MeSH Terms :
Calcium-Binding Proteins/*metabolism
Fatty Liver/*metabolism
Proto-Oncogene Proteins c-akt/*metabolism
Receptor for Advanced Glycation End Products/*metabolism
S100 Proteins/*metabolism
Signal Transduction/*physiology
TOR Serine-Threonine Kinases/*metabolism
Adult ; Animals ; Carcinoma, Hepatocellular/metabolism ; Cell Line ; Disease Models, Animal ; Female ; Humans ; Lipid Metabolism/physiology ; Lipogenesis/physiology ; Liver/metabolism ; Liver Neoplasms/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Non-alcoholic Fatty Liver Disease/metabolism
Contributed Indexing :
Keywords: AKT*; Lipid metabolism*; Obesity, NAFLD*; S100A11*; mTOR*
Substance Nomenclature :
0 (AGER protein, human)
0 (Calcium-Binding Proteins)
0 (Receptor for Advanced Glycation End Products)
0 (S100 Proteins)
146909-89-9 (S100A11 protein, human)
EC 2.7.1.1 (MTOR protein, human)
EC 2.7.1.1 (TOR Serine-Threonine Kinases)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
Entry Date(s) :
Date Created: 20210211 Date Completed: 20210405 Latest Revision: 20210405
Update Code :
20210406
DOI :
10.1016/j.metabol.2021.154725
PMID :
33571540
Czasopismo naukowe
Rationale: Nonalcoholic fatty liver disease (NAFLD), the most common cause of chronic liver disease, has become an increasingly severe public health problem. However, the underlying mechanism for the occurrence and development of NAFLD remains largely unknown. S100 calcium-binding protein A11 (S100A11) is a multifunctional protein previously reported to be a poor prognostic indicator of hepatocellular carcinoma, while the role of S100A11 affects NAFLD is still not clear.
Methods: Immunohistochemical staining was performed using human NAFLD and control biopsy specimens. Serum level of S100A11 were analyzed by Elisa assays. The S100A11 over-expressed/ knocked-down model was established in vitro or in vivo. The expression levels of genes related to lipid metabolism in liver tissue were performed by quantitative PCR and western blotting. Hepatic lipid accumulation was determined by biochemical measurements and histochemistry.
Results: We showed that the concentration of serum S100A11 was significantly elevated in NAFLD patients, and expression of S100A11 was remarkedly increased in the livers of NAFLD patients and mouse models. Overexpression of S100A11 in vivo markedly increased liver steatosis, body weight, and serum aspartate aminotransaminase (AST) levels. Mechanistically, our results demonstrated that S100A11 acted as a positive regulator of AKT/mTOR signaling to induce lipid synthesis and aggravate lipid deposition.
Conclusions: These results provide evidence for a novel role of S100A11 that contributes to hepatic steatosis, suggesting that targeting S100A11 may be an alternative approach for the treatment of NAFLD.
(Copyright © 2021 Elsevier Inc. All rights reserved.)

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