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MiR-455 targeting SOCS3 improve liver lipid disorders in diabetic mice
MiR-455 has been verified a key regulator of brown adipose tissue and adipose tissue-specific overexpression of miR-455 (ap2-miR-455) mice could combat high-fat-diet-induced obesity. This study is to verify overexpression of miR-455 could ameliorate the lipid accumulation and metabolism in the liver...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7153657/ https://www.ncbi.nlm.nih.gov/pubmed/32272865 http://dx.doi.org/10.1080/21623945.2020.1749495 |
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author | Fang, Shu Feng, Jie Zhang, Hongbin Li, Ping Zhang, Yudan Zeng, Yanmei Cai, Yingying Lin, Xiaochun Xue, Yaoming Guan, Meiping |
author_facet | Fang, Shu Feng, Jie Zhang, Hongbin Li, Ping Zhang, Yudan Zeng, Yanmei Cai, Yingying Lin, Xiaochun Xue, Yaoming Guan, Meiping |
author_sort | Fang, Shu |
collection | PubMed |
description | MiR-455 has been verified a key regulator of brown adipose tissue and adipose tissue-specific overexpression of miR-455 (ap2-miR-455) mice could combat high-fat-diet-induced obesity. This study is to verify overexpression of miR-455 could ameliorate the lipid accumulation and metabolism in the liver of db/db diabetic mice and explore the potential mechanisms. Diabetic mice (db/db) and control mice (db/m) were randomly divided into four groups. After overexpression of miR-455 in the liver of db/db mice, the triglycerides level in both serum and liver decreased, the lipid deposit in liver was improved, the expression of fatty acid synthase, stearoyl-CoA desaturase 1, sterol regulatory element binding protein 1c (SREBP-1c) and acetyl-CoA carboxylase (ACCα) was also significantly down-regulated. TargetScan indicated that suppressor of cytokine signalling 3 (SOCS3) is predicated to target miR-455 and the protein of SOCS3 in the liver of db/db mice after intervention was significantly decreased. The dual luciferase reporter assay showed that SOCS3 was target gene of miR-455. In vitro, in Palmitate (PA)-stimulated human normal liver (LO2) cells, transfected miR-455 mimic could significantly inhibit the expression of SOCS3, while transfected miR-455 inhibitor could up-regulate the expression of SOCS3. Transfecting LO2 cells with siRNA of SOCS3 could significantly down-regulate the protein expression of SREBP-1c and ACCα. Our study showed that overexpression of miR-455 in the liver could improve lipid metabolism in diabetic mice by down-regulating its target gene SOCS3. |
format | Online Article Text |
id | pubmed-7153657 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-71536572020-04-16 MiR-455 targeting SOCS3 improve liver lipid disorders in diabetic mice Fang, Shu Feng, Jie Zhang, Hongbin Li, Ping Zhang, Yudan Zeng, Yanmei Cai, Yingying Lin, Xiaochun Xue, Yaoming Guan, Meiping Adipocyte Research Article MiR-455 has been verified a key regulator of brown adipose tissue and adipose tissue-specific overexpression of miR-455 (ap2-miR-455) mice could combat high-fat-diet-induced obesity. This study is to verify overexpression of miR-455 could ameliorate the lipid accumulation and metabolism in the liver of db/db diabetic mice and explore the potential mechanisms. Diabetic mice (db/db) and control mice (db/m) were randomly divided into four groups. After overexpression of miR-455 in the liver of db/db mice, the triglycerides level in both serum and liver decreased, the lipid deposit in liver was improved, the expression of fatty acid synthase, stearoyl-CoA desaturase 1, sterol regulatory element binding protein 1c (SREBP-1c) and acetyl-CoA carboxylase (ACCα) was also significantly down-regulated. TargetScan indicated that suppressor of cytokine signalling 3 (SOCS3) is predicated to target miR-455 and the protein of SOCS3 in the liver of db/db mice after intervention was significantly decreased. The dual luciferase reporter assay showed that SOCS3 was target gene of miR-455. In vitro, in Palmitate (PA)-stimulated human normal liver (LO2) cells, transfected miR-455 mimic could significantly inhibit the expression of SOCS3, while transfected miR-455 inhibitor could up-regulate the expression of SOCS3. Transfecting LO2 cells with siRNA of SOCS3 could significantly down-regulate the protein expression of SREBP-1c and ACCα. Our study showed that overexpression of miR-455 in the liver could improve lipid metabolism in diabetic mice by down-regulating its target gene SOCS3. Taylor & Francis 2020-04-09 /pmc/articles/PMC7153657/ /pubmed/32272865 http://dx.doi.org/10.1080/21623945.2020.1749495 Text en © 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Fang, Shu Feng, Jie Zhang, Hongbin Li, Ping Zhang, Yudan Zeng, Yanmei Cai, Yingying Lin, Xiaochun Xue, Yaoming Guan, Meiping MiR-455 targeting SOCS3 improve liver lipid disorders in diabetic mice |
title | MiR-455 targeting SOCS3 improve liver lipid disorders in diabetic mice |
title_full | MiR-455 targeting SOCS3 improve liver lipid disorders in diabetic mice |
title_fullStr | MiR-455 targeting SOCS3 improve liver lipid disorders in diabetic mice |
title_full_unstemmed | MiR-455 targeting SOCS3 improve liver lipid disorders in diabetic mice |
title_short | MiR-455 targeting SOCS3 improve liver lipid disorders in diabetic mice |
title_sort | mir-455 targeting socs3 improve liver lipid disorders in diabetic mice |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7153657/ https://www.ncbi.nlm.nih.gov/pubmed/32272865 http://dx.doi.org/10.1080/21623945.2020.1749495 |
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