Differential expression of microRNAs in mouse pain models

<p>Abstract</p> <p>Background</p> <p>MicroRNAs (miRNAs) are short non-coding RNAs that inhibit translation of target genes by binding to their mRNAs. The expression of numerous brain-specific miRNAs with a high degree of temporal and spatial specificity suggests that mi...

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Main Authors: De Lucca Fernando L, Zanon Sônia, Sousa Thais A, Ravanelli Maria I, Cadetti Flaviane, Kusuda Ricardo, Lucas Guilherme
Format: Article
Language:English
Published: SAGE Publishing 2011-03-01
Series:Molecular Pain
Online Access:http://www.molecularpain.com/content/7/1/17
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spelling doaj-a8a26fd330af42c3a6927c19ed3f62822020-11-25T03:11:11ZengSAGE PublishingMolecular Pain1744-80692011-03-01711710.1186/1744-8069-7-17Differential expression of microRNAs in mouse pain modelsDe Lucca Fernando LZanon SôniaSousa Thais ARavanelli Maria ICadetti FlavianeKusuda RicardoLucas Guilherme<p>Abstract</p> <p>Background</p> <p>MicroRNAs (miRNAs) are short non-coding RNAs that inhibit translation of target genes by binding to their mRNAs. The expression of numerous brain-specific miRNAs with a high degree of temporal and spatial specificity suggests that miRNAs play an important role in gene regulation in health and disease. Here we investigate the time course gene expression profile of miR-1, -16, and -206 in mouse dorsal root ganglion (DRG), and spinal cord dorsal horn under inflammatory and neuropathic pain conditions as well as following acute noxious stimulation.</p> <p>Results</p> <p>Quantitative real-time polymerase chain reaction analyses showed that the mature form of miR-1, -16 and -206, is expressed in DRG and the dorsal horn of the spinal cord. Moreover, CFA-induced inflammation significantly reduced miRs-1 and -16 expression in DRG whereas miR-206 was downregulated in a time dependent manner. Conversely, in the spinal dorsal horn all three miRNAs monitored were upregulated. After sciatic nerve partial ligation, miR-1 and -206 were downregulated in DRG with no change in the spinal dorsal horn. On the other hand, axotomy increases the relative expression of miR-1, -16, and 206 in a time-dependent fashion while in the dorsal horn there was a significant downregulation of miR-1. Acute noxious stimulation with capsaicin also increased the expression of miR-1 and -16 in DRG cells but, on the other hand, in the spinal dorsal horn only a high dose of capsaicin was able to downregulate miR-206 expression.</p> <p>Conclusions</p> <p>Our results indicate that miRNAs may participate in the regulatory mechanisms of genes associated with the pathophysiology of chronic pain as well as the nociceptive processing following acute noxious stimulation. We found substantial evidence that miRNAs are differentially regulated in DRG and the dorsal horn of the spinal cord under different pain states. Therefore, miRNA expression in the nociceptive system shows not only temporal and spatial specificity but is also stimulus-dependent.</p> http://www.molecularpain.com/content/7/1/17
collection DOAJ
language English
format Article
sources DOAJ
author De Lucca Fernando L
Zanon Sônia
Sousa Thais A
Ravanelli Maria I
Cadetti Flaviane
Kusuda Ricardo
Lucas Guilherme
spellingShingle De Lucca Fernando L
Zanon Sônia
Sousa Thais A
Ravanelli Maria I
Cadetti Flaviane
Kusuda Ricardo
Lucas Guilherme
Differential expression of microRNAs in mouse pain models
Molecular Pain
author_facet De Lucca Fernando L
Zanon Sônia
Sousa Thais A
Ravanelli Maria I
Cadetti Flaviane
Kusuda Ricardo
Lucas Guilherme
author_sort De Lucca Fernando L
title Differential expression of microRNAs in mouse pain models
title_short Differential expression of microRNAs in mouse pain models
title_full Differential expression of microRNAs in mouse pain models
title_fullStr Differential expression of microRNAs in mouse pain models
title_full_unstemmed Differential expression of microRNAs in mouse pain models
title_sort differential expression of micrornas in mouse pain models
publisher SAGE Publishing
series Molecular Pain
issn 1744-8069
publishDate 2011-03-01
description <p>Abstract</p> <p>Background</p> <p>MicroRNAs (miRNAs) are short non-coding RNAs that inhibit translation of target genes by binding to their mRNAs. The expression of numerous brain-specific miRNAs with a high degree of temporal and spatial specificity suggests that miRNAs play an important role in gene regulation in health and disease. Here we investigate the time course gene expression profile of miR-1, -16, and -206 in mouse dorsal root ganglion (DRG), and spinal cord dorsal horn under inflammatory and neuropathic pain conditions as well as following acute noxious stimulation.</p> <p>Results</p> <p>Quantitative real-time polymerase chain reaction analyses showed that the mature form of miR-1, -16 and -206, is expressed in DRG and the dorsal horn of the spinal cord. Moreover, CFA-induced inflammation significantly reduced miRs-1 and -16 expression in DRG whereas miR-206 was downregulated in a time dependent manner. Conversely, in the spinal dorsal horn all three miRNAs monitored were upregulated. After sciatic nerve partial ligation, miR-1 and -206 were downregulated in DRG with no change in the spinal dorsal horn. On the other hand, axotomy increases the relative expression of miR-1, -16, and 206 in a time-dependent fashion while in the dorsal horn there was a significant downregulation of miR-1. Acute noxious stimulation with capsaicin also increased the expression of miR-1 and -16 in DRG cells but, on the other hand, in the spinal dorsal horn only a high dose of capsaicin was able to downregulate miR-206 expression.</p> <p>Conclusions</p> <p>Our results indicate that miRNAs may participate in the regulatory mechanisms of genes associated with the pathophysiology of chronic pain as well as the nociceptive processing following acute noxious stimulation. We found substantial evidence that miRNAs are differentially regulated in DRG and the dorsal horn of the spinal cord under different pain states. Therefore, miRNA expression in the nociceptive system shows not only temporal and spatial specificity but is also stimulus-dependent.</p>
url http://www.molecularpain.com/content/7/1/17
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