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miR-29a modulates SCD expression and is regulated in response to a saturated fatty acid diet in juvenile genetically improved farmed tilapia (Oreochromis niloticus)
MicroRNAs (miRNAs) are small non-coding RNAs that regulate target gene expression by binding to the 3′ untranslated region (3′ UTR) of the target mRNA. MiRNAs regulate a large variety of genes, including those involved in liver biology and disease. Here, we report for the first time that miR-29a pos...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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The Company of Biologists Ltd
2017
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5413068/ https://www.ncbi.nlm.nih.gov/pubmed/28167804 http://dx.doi.org/10.1242/jeb.151506 |
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author | Qiang, Jun Tao, Yi Fan He, Jie Sun, Yi Lan Xu, Pao |
author_facet | Qiang, Jun Tao, Yi Fan He, Jie Sun, Yi Lan Xu, Pao |
author_sort | Qiang, Jun |
collection | PubMed |
description | MicroRNAs (miRNAs) are small non-coding RNAs that regulate target gene expression by binding to the 3′ untranslated region (3′ UTR) of the target mRNA. MiRNAs regulate a large variety of genes, including those involved in liver biology and disease. Here, we report for the first time that miR-29a post-transcriptionally regulates stearoyl-CoA desaturase (SCD) by binding to its 3′ UTR in genetically improved farmed tilapia (GIFT), Oreochromis niloticus, as shown by a 3′ UTR luciferase reporter assay. miR-29a antagomir treatment in vivo resulted in significant upregulation of SCD expression. We found that miR-29a expression was negatively correlated with SCD expression in GIFT liver. Inhibition of miR-29a led to a significant increase in SCD expression on day 60 induced by a saturated fatty acid diet, thereby increasing conversion of 16:0 and 18:0 to 16:1 and 18:1, respectively, and activating serum insulin, which would favor glucose and lipid uptake by the liver. These results indicate that miR-29a regulates SCD levels by binding to its 3′ UTR, and this interaction affects saturated fatty acid stress induction and insulin and lipid accumulation in serum. Our results suggest that miR-29a is critical in regulating lipid metabolism homeostasis in GIFT liver, and this might provide a basis for understanding the biological processes and therapeutic intervention encountered in fatty liver. |
format | Online Article Text |
id | pubmed-5413068 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | The Company of Biologists Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-54130682017-05-16 miR-29a modulates SCD expression and is regulated in response to a saturated fatty acid diet in juvenile genetically improved farmed tilapia (Oreochromis niloticus) Qiang, Jun Tao, Yi Fan He, Jie Sun, Yi Lan Xu, Pao J Exp Biol Research Article MicroRNAs (miRNAs) are small non-coding RNAs that regulate target gene expression by binding to the 3′ untranslated region (3′ UTR) of the target mRNA. MiRNAs regulate a large variety of genes, including those involved in liver biology and disease. Here, we report for the first time that miR-29a post-transcriptionally regulates stearoyl-CoA desaturase (SCD) by binding to its 3′ UTR in genetically improved farmed tilapia (GIFT), Oreochromis niloticus, as shown by a 3′ UTR luciferase reporter assay. miR-29a antagomir treatment in vivo resulted in significant upregulation of SCD expression. We found that miR-29a expression was negatively correlated with SCD expression in GIFT liver. Inhibition of miR-29a led to a significant increase in SCD expression on day 60 induced by a saturated fatty acid diet, thereby increasing conversion of 16:0 and 18:0 to 16:1 and 18:1, respectively, and activating serum insulin, which would favor glucose and lipid uptake by the liver. These results indicate that miR-29a regulates SCD levels by binding to its 3′ UTR, and this interaction affects saturated fatty acid stress induction and insulin and lipid accumulation in serum. Our results suggest that miR-29a is critical in regulating lipid metabolism homeostasis in GIFT liver, and this might provide a basis for understanding the biological processes and therapeutic intervention encountered in fatty liver. The Company of Biologists Ltd 2017-04-15 /pmc/articles/PMC5413068/ /pubmed/28167804 http://dx.doi.org/10.1242/jeb.151506 Text en © 2017. Published by The Company of Biologists Ltd http://creativecommons.org/licenses/by/3.0This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. |
spellingShingle | Research Article Qiang, Jun Tao, Yi Fan He, Jie Sun, Yi Lan Xu, Pao miR-29a modulates SCD expression and is regulated in response to a saturated fatty acid diet in juvenile genetically improved farmed tilapia (Oreochromis niloticus) |
title | miR-29a modulates SCD expression and is regulated in response to a saturated fatty acid diet in juvenile genetically improved farmed tilapia (Oreochromis niloticus) |
title_full | miR-29a modulates SCD expression and is regulated in response to a saturated fatty acid diet in juvenile genetically improved farmed tilapia (Oreochromis niloticus) |
title_fullStr | miR-29a modulates SCD expression and is regulated in response to a saturated fatty acid diet in juvenile genetically improved farmed tilapia (Oreochromis niloticus) |
title_full_unstemmed | miR-29a modulates SCD expression and is regulated in response to a saturated fatty acid diet in juvenile genetically improved farmed tilapia (Oreochromis niloticus) |
title_short | miR-29a modulates SCD expression and is regulated in response to a saturated fatty acid diet in juvenile genetically improved farmed tilapia (Oreochromis niloticus) |
title_sort | mir-29a modulates scd expression and is regulated in response to a saturated fatty acid diet in juvenile genetically improved farmed tilapia (oreochromis niloticus) |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5413068/ https://www.ncbi.nlm.nih.gov/pubmed/28167804 http://dx.doi.org/10.1242/jeb.151506 |
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