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Acute Stress Alters Amygdala microRNA miR-135a and miR-124 Expression: Inferences for Corticosteroid Dependent Stress Response
The amygdala is a brain structure considered a key node for the regulation of neuroendocrine stress response. Stress-induced response in amygdala is accomplished through neurotransmitter activation and an alteration of gene expression. MicroRNAs (miRNAs) are important regulators of gene expression i...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3762773/ https://www.ncbi.nlm.nih.gov/pubmed/24023867 http://dx.doi.org/10.1371/journal.pone.0073385 |
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author | Mannironi, Cecilia Camon, Jeremy De Vito, Francesca Biundo, Antonio De Stefano, Maria Egle Persiconi, Irene Bozzoni, Irene Fragapane, Paola Mele, Andrea Presutti, Carlo |
author_facet | Mannironi, Cecilia Camon, Jeremy De Vito, Francesca Biundo, Antonio De Stefano, Maria Egle Persiconi, Irene Bozzoni, Irene Fragapane, Paola Mele, Andrea Presutti, Carlo |
author_sort | Mannironi, Cecilia |
collection | PubMed |
description | The amygdala is a brain structure considered a key node for the regulation of neuroendocrine stress response. Stress-induced response in amygdala is accomplished through neurotransmitter activation and an alteration of gene expression. MicroRNAs (miRNAs) are important regulators of gene expression in the nervous system and are very well suited effectors of stress response for their ability to reversibly silence specific mRNAs. In order to study how acute stress affects miRNAs expression in amygdala we analyzed the miRNA profile after two hours of mouse restraint, by microarray analysis and reverse transcription real time PCR. We found that miR-135a and miR-124 were negatively regulated. Among in silico predicted targets we identified the mineralocorticoid receptor (MR) as a target of both miR-135a and miR-124. Luciferase experiments and endogenous protein expression analysis upon miRNA upregulation and inhibition allowed us to demonstrate that mir-135a and mir-124 are able to negatively affect the expression of the MR. The increased levels of the amygdala MR protein after two hours of restraint, that we analyzed by western blot, negatively correlate with miR-135a and miR-124 expression. These findings point to a role of miR-135a and miR-124 in acute stress as regulators of the MR, an important effector of early stress response. |
format | Online Article Text |
id | pubmed-3762773 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-37627732013-09-10 Acute Stress Alters Amygdala microRNA miR-135a and miR-124 Expression: Inferences for Corticosteroid Dependent Stress Response Mannironi, Cecilia Camon, Jeremy De Vito, Francesca Biundo, Antonio De Stefano, Maria Egle Persiconi, Irene Bozzoni, Irene Fragapane, Paola Mele, Andrea Presutti, Carlo PLoS One Research Article The amygdala is a brain structure considered a key node for the regulation of neuroendocrine stress response. Stress-induced response in amygdala is accomplished through neurotransmitter activation and an alteration of gene expression. MicroRNAs (miRNAs) are important regulators of gene expression in the nervous system and are very well suited effectors of stress response for their ability to reversibly silence specific mRNAs. In order to study how acute stress affects miRNAs expression in amygdala we analyzed the miRNA profile after two hours of mouse restraint, by microarray analysis and reverse transcription real time PCR. We found that miR-135a and miR-124 were negatively regulated. Among in silico predicted targets we identified the mineralocorticoid receptor (MR) as a target of both miR-135a and miR-124. Luciferase experiments and endogenous protein expression analysis upon miRNA upregulation and inhibition allowed us to demonstrate that mir-135a and mir-124 are able to negatively affect the expression of the MR. The increased levels of the amygdala MR protein after two hours of restraint, that we analyzed by western blot, negatively correlate with miR-135a and miR-124 expression. These findings point to a role of miR-135a and miR-124 in acute stress as regulators of the MR, an important effector of early stress response. Public Library of Science 2013-09-04 /pmc/articles/PMC3762773/ /pubmed/24023867 http://dx.doi.org/10.1371/journal.pone.0073385 Text en © 2013 Mannironi et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Mannironi, Cecilia Camon, Jeremy De Vito, Francesca Biundo, Antonio De Stefano, Maria Egle Persiconi, Irene Bozzoni, Irene Fragapane, Paola Mele, Andrea Presutti, Carlo Acute Stress Alters Amygdala microRNA miR-135a and miR-124 Expression: Inferences for Corticosteroid Dependent Stress Response |
title | Acute Stress Alters Amygdala microRNA miR-135a and miR-124 Expression: Inferences for Corticosteroid Dependent Stress Response |
title_full | Acute Stress Alters Amygdala microRNA miR-135a and miR-124 Expression: Inferences for Corticosteroid Dependent Stress Response |
title_fullStr | Acute Stress Alters Amygdala microRNA miR-135a and miR-124 Expression: Inferences for Corticosteroid Dependent Stress Response |
title_full_unstemmed | Acute Stress Alters Amygdala microRNA miR-135a and miR-124 Expression: Inferences for Corticosteroid Dependent Stress Response |
title_short | Acute Stress Alters Amygdala microRNA miR-135a and miR-124 Expression: Inferences for Corticosteroid Dependent Stress Response |
title_sort | acute stress alters amygdala microrna mir-135a and mir-124 expression: inferences for corticosteroid dependent stress response |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3762773/ https://www.ncbi.nlm.nih.gov/pubmed/24023867 http://dx.doi.org/10.1371/journal.pone.0073385 |
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