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MiR-184 regulates insulin secretion through repression of Slc25a22
Insulin secretion from pancreatic β-cells plays an essential role in blood glucose homeostasis and type 2 diabetes. Many genes are involved in the secretion of insulin and most of these genes can be targeted by microRNAs (miRNAs). However, the role of miRNAs in insulin secretion and type 2 diabetes...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
PeerJ Inc.
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3792180/ https://www.ncbi.nlm.nih.gov/pubmed/24109547 http://dx.doi.org/10.7717/peerj.162 |
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author | Morita, Sumiyo Horii, Takuro Kimura, Mika Hatada, Izuho |
author_facet | Morita, Sumiyo Horii, Takuro Kimura, Mika Hatada, Izuho |
author_sort | Morita, Sumiyo |
collection | PubMed |
description | Insulin secretion from pancreatic β-cells plays an essential role in blood glucose homeostasis and type 2 diabetes. Many genes are involved in the secretion of insulin and most of these genes can be targeted by microRNAs (miRNAs). However, the role of miRNAs in insulin secretion and type 2 diabetes has not been exhaustively studied. The expression miR-184, a miRNA enriched in pancreatic islets, negatively correlates with insulin secretion, suggesting that it is a good candidate for miRNA-mediated regulation of insulin secretion. Here we report that miR-184 inhibits insulin secretion in the MIN6 pancreatic β-cell line through the repression of its target Slc25a22, a mitochondrial glutamate carrier. Our study provides new insight into the regulation of insulin secretion by glutamate transport in mitochondria. |
format | Online Article Text |
id | pubmed-3792180 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | PeerJ Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-37921802013-10-09 MiR-184 regulates insulin secretion through repression of Slc25a22 Morita, Sumiyo Horii, Takuro Kimura, Mika Hatada, Izuho PeerJ Genomics Insulin secretion from pancreatic β-cells plays an essential role in blood glucose homeostasis and type 2 diabetes. Many genes are involved in the secretion of insulin and most of these genes can be targeted by microRNAs (miRNAs). However, the role of miRNAs in insulin secretion and type 2 diabetes has not been exhaustively studied. The expression miR-184, a miRNA enriched in pancreatic islets, negatively correlates with insulin secretion, suggesting that it is a good candidate for miRNA-mediated regulation of insulin secretion. Here we report that miR-184 inhibits insulin secretion in the MIN6 pancreatic β-cell line through the repression of its target Slc25a22, a mitochondrial glutamate carrier. Our study provides new insight into the regulation of insulin secretion by glutamate transport in mitochondria. PeerJ Inc. 2013-09-24 /pmc/articles/PMC3792180/ /pubmed/24109547 http://dx.doi.org/10.7717/peerj.162 Text en © 2013 Morita et al. http://creativecommons.org/licenses/by/3.0/ This 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 the original author and source are credited. |
spellingShingle | Genomics Morita, Sumiyo Horii, Takuro Kimura, Mika Hatada, Izuho MiR-184 regulates insulin secretion through repression of Slc25a22 |
title | MiR-184 regulates insulin secretion through repression of Slc25a22 |
title_full | MiR-184 regulates insulin secretion through repression of Slc25a22 |
title_fullStr | MiR-184 regulates insulin secretion through repression of Slc25a22 |
title_full_unstemmed | MiR-184 regulates insulin secretion through repression of Slc25a22 |
title_short | MiR-184 regulates insulin secretion through repression of Slc25a22 |
title_sort | mir-184 regulates insulin secretion through repression of slc25a22 |
topic | Genomics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3792180/ https://www.ncbi.nlm.nih.gov/pubmed/24109547 http://dx.doi.org/10.7717/peerj.162 |
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