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PUFA diets alter the microRNA expression profiles in an inflammation rat model

Omega-3 and -6 polyunsaturated fatty acids (PUFAs) can directly or indirectly regulate immune homeostasis via inflammatory pathways, and components of these pathways are crucial targets of microRNAs (miRNAs). However, no study has examined the changes in the miRNA transcriptome during PUFA-regulated...

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Autores principales: ZHENG, ZHENG, GE, YINLIN, ZHANG, JINYU, XUE, MEILAN, LI, QUAN, LIN, DONGLIANG, MA, WENHUI
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4394972/
https://www.ncbi.nlm.nih.gov/pubmed/25672643
http://dx.doi.org/10.3892/mmr.2015.3318
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author ZHENG, ZHENG
GE, YINLIN
ZHANG, JINYU
XUE, MEILAN
LI, QUAN
LIN, DONGLIANG
MA, WENHUI
author_facet ZHENG, ZHENG
GE, YINLIN
ZHANG, JINYU
XUE, MEILAN
LI, QUAN
LIN, DONGLIANG
MA, WENHUI
author_sort ZHENG, ZHENG
collection PubMed
description Omega-3 and -6 polyunsaturated fatty acids (PUFAs) can directly or indirectly regulate immune homeostasis via inflammatory pathways, and components of these pathways are crucial targets of microRNAs (miRNAs). However, no study has examined the changes in the miRNA transcriptome during PUFA-regulated inflammatory processes. Here, we established PUFA diet-induced autoimmune-prone (AP) and autoimmune-averse (AA) rat models, and studied their physical characteristics and immune status. Additionally, miRNA expression patterns in the rat models were compared using microarray assays and bioinformatic methods. A total of 54 miRNAs were differentially expressed in common between the AP and the AA rats, and the changes in rno-miR-19b-3p, -146b-5p and -183-5p expression were validated using stem-loop reverse transcription-quantitative polymerase chain reaction. To better understand the mechanisms underlying PUFA-regulated miRNA changes during inflammation, computational algorithms and biological databases were used to identify the target genes of the three validated miRNAs. Furthermore, Gene Ontology (GO) term annotation and KEGG pathway analyses of the miRNA targets further allowed to explore the potential implication of the miRNAs in inflammatory pathways. The predicted PUFA-regulated inflammatory pathways included the Toll-like receptor (TLR), T cell receptor (TCR), NOD-like receptor (NLR), RIG-I-like receptor (RLR), mitogen-activated protein kinase (MAPK) and the transforming growth factor-β (TGF-β) pathway. This study is the first report, to the best of our knowledge, on in vivo comparative profiling of miRNA transcriptomes in PUFA diet-induced inflammatory rat models using a microarray approach. The results provide a useful resource for future investigation of the role of PUFA-regulated miRNAs in immune homeostasis.
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spelling pubmed-43949722015-04-17 PUFA diets alter the microRNA expression profiles in an inflammation rat model ZHENG, ZHENG GE, YINLIN ZHANG, JINYU XUE, MEILAN LI, QUAN LIN, DONGLIANG MA, WENHUI Mol Med Rep Articles Omega-3 and -6 polyunsaturated fatty acids (PUFAs) can directly or indirectly regulate immune homeostasis via inflammatory pathways, and components of these pathways are crucial targets of microRNAs (miRNAs). However, no study has examined the changes in the miRNA transcriptome during PUFA-regulated inflammatory processes. Here, we established PUFA diet-induced autoimmune-prone (AP) and autoimmune-averse (AA) rat models, and studied their physical characteristics and immune status. Additionally, miRNA expression patterns in the rat models were compared using microarray assays and bioinformatic methods. A total of 54 miRNAs were differentially expressed in common between the AP and the AA rats, and the changes in rno-miR-19b-3p, -146b-5p and -183-5p expression were validated using stem-loop reverse transcription-quantitative polymerase chain reaction. To better understand the mechanisms underlying PUFA-regulated miRNA changes during inflammation, computational algorithms and biological databases were used to identify the target genes of the three validated miRNAs. Furthermore, Gene Ontology (GO) term annotation and KEGG pathway analyses of the miRNA targets further allowed to explore the potential implication of the miRNAs in inflammatory pathways. The predicted PUFA-regulated inflammatory pathways included the Toll-like receptor (TLR), T cell receptor (TCR), NOD-like receptor (NLR), RIG-I-like receptor (RLR), mitogen-activated protein kinase (MAPK) and the transforming growth factor-β (TGF-β) pathway. This study is the first report, to the best of our knowledge, on in vivo comparative profiling of miRNA transcriptomes in PUFA diet-induced inflammatory rat models using a microarray approach. The results provide a useful resource for future investigation of the role of PUFA-regulated miRNAs in immune homeostasis. D.A. Spandidos 2015-06 2015-02-09 /pmc/articles/PMC4394972/ /pubmed/25672643 http://dx.doi.org/10.3892/mmr.2015.3318 Text en Copyright © 2015, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Articles
ZHENG, ZHENG
GE, YINLIN
ZHANG, JINYU
XUE, MEILAN
LI, QUAN
LIN, DONGLIANG
MA, WENHUI
PUFA diets alter the microRNA expression profiles in an inflammation rat model
title PUFA diets alter the microRNA expression profiles in an inflammation rat model
title_full PUFA diets alter the microRNA expression profiles in an inflammation rat model
title_fullStr PUFA diets alter the microRNA expression profiles in an inflammation rat model
title_full_unstemmed PUFA diets alter the microRNA expression profiles in an inflammation rat model
title_short PUFA diets alter the microRNA expression profiles in an inflammation rat model
title_sort pufa diets alter the microrna expression profiles in an inflammation rat model
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4394972/
https://www.ncbi.nlm.nih.gov/pubmed/25672643
http://dx.doi.org/10.3892/mmr.2015.3318
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