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MiR-184 regulates pancreatic β-cell function according to glucose metabolism.

Tattikota, Sudhir G; Rathjen, Thomas; Hausser, Jean; Khedkar, Aditya; Kabra, Uma D; Pandey, Varun K; Sury, Matthias; Wessels, Hans-Hermann; Mollet, Ines LU and Eliasson, Lena LU , et al. (2015) In Journal of Biological Chemistry 290(33). p.20284-20294
Abstract
In response to fasting or hyperglycemia, the pancreatic β-cell alters its output of secreted insulin; however the pathways governing this adaptive response are not entirely established. While the precise role of microRNAs (miRNAs) is also unclear, a recurring theme emphasizes their function in cellular stress responses. We recently showed that miR-184, an abundant miRNA in the β-cell, regulates compensatory proliferation and secretion during insulin resistance. Consistent with previous studies showing miR-184 suppresses insulin release, expression of this miRNA was increased in islets after fasting, demonstrating an active role in the β-cell as glucose levels lower and the insulin demand ceases. Additionally, miR-184 was negatively... (More)
In response to fasting or hyperglycemia, the pancreatic β-cell alters its output of secreted insulin; however the pathways governing this adaptive response are not entirely established. While the precise role of microRNAs (miRNAs) is also unclear, a recurring theme emphasizes their function in cellular stress responses. We recently showed that miR-184, an abundant miRNA in the β-cell, regulates compensatory proliferation and secretion during insulin resistance. Consistent with previous studies showing miR-184 suppresses insulin release, expression of this miRNA was increased in islets after fasting, demonstrating an active role in the β-cell as glucose levels lower and the insulin demand ceases. Additionally, miR-184 was negatively regulated upon administration of a sucrose-rich diet in Drosophila demonstrating strong conservation of this pathway through evolution. Furthermore, miR-184 and its target Argonaute2 (Ago2) remained inversely correlated as concentrations of extracellular glucose increased, underlining a functional relationship between this miRNA and its targets. Lastly, restoration of Ago2 in the presence of miR-184 rescued suppression of miR-375-targeted genes suggesting these genes act in a coordinated manner during changes in the metabolic context. Together, these results highlight the adaptive role of miR-184 according to glucose metabolism and suggest the regulatory role of this miRNA in energy homeostasis is highly conserved. (Less)
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Contribution to journal
publication status
published
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Journal of Biological Chemistry
volume
290
issue
33
pages
20284 - 20294
publisher
ASBMB
external identifiers
  • pmid:26152724
  • wos:000359608900028
  • scopus:84939825167
ISSN
1083-351X
DOI
10.1074/jbc.M115.658625
language
English
LU publication?
yes
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2b90dd2a-4af7-4152-83c5-cf5812fba127 (old id 7750172)
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http://www.ncbi.nlm.nih.gov/pubmed/26152724?dopt=Abstract
date added to LUP
2015-08-07 00:19:51
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2017-11-19 03:02:56
@article{2b90dd2a-4af7-4152-83c5-cf5812fba127,
  abstract     = {In response to fasting or hyperglycemia, the pancreatic β-cell alters its output of secreted insulin; however the pathways governing this adaptive response are not entirely established. While the precise role of microRNAs (miRNAs) is also unclear, a recurring theme emphasizes their function in cellular stress responses. We recently showed that miR-184, an abundant miRNA in the β-cell, regulates compensatory proliferation and secretion during insulin resistance. Consistent with previous studies showing miR-184 suppresses insulin release, expression of this miRNA was increased in islets after fasting, demonstrating an active role in the β-cell as glucose levels lower and the insulin demand ceases. Additionally, miR-184 was negatively regulated upon administration of a sucrose-rich diet in Drosophila demonstrating strong conservation of this pathway through evolution. Furthermore, miR-184 and its target Argonaute2 (Ago2) remained inversely correlated as concentrations of extracellular glucose increased, underlining a functional relationship between this miRNA and its targets. Lastly, restoration of Ago2 in the presence of miR-184 rescued suppression of miR-375-targeted genes suggesting these genes act in a coordinated manner during changes in the metabolic context. Together, these results highlight the adaptive role of miR-184 according to glucose metabolism and suggest the regulatory role of this miRNA in energy homeostasis is highly conserved.},
  author       = {Tattikota, Sudhir G and Rathjen, Thomas and Hausser, Jean and Khedkar, Aditya and Kabra, Uma D and Pandey, Varun K and Sury, Matthias and Wessels, Hans-Hermann and Mollet, Ines and Eliasson, Lena and Selbach, Matthias and Zinzen, Robert P and Zavolan, Mihaela and Kadener, Sebastian and Tschöp, Matthias and Jastroch, Martin and Friedländer, Marc R and Poy, Matthew N},
  issn         = {1083-351X},
  language     = {eng},
  number       = {33},
  pages        = {20284--20294},
  publisher    = {ASBMB},
  series       = {Journal of Biological Chemistry},
  title        = {MiR-184 regulates pancreatic β-cell function according to glucose metabolism.},
  url          = {http://dx.doi.org/10.1074/jbc.M115.658625},
  volume       = {290},
  year         = {2015},
}