Literature DB >> 27939730

Viral MicroRNAs Identified in Human Dental Pulp.

Sheng Zhong1, Afsar Naqvi2, Eric Bair3, Salvador Nares2, Asma A Khan4.   

Abstract

INTRODUCTION: MicroRNAs (miRs) are a family of noncoding RNAs that regulate gene expression. They are ubiquitous among multicellular eukaryotes and are also encoded by some viruses. Upon infection, viral miRs (vmiRs) can potentially target gene expression in the host and alter the immune response. Although prior studies have reported viral infections in human pulp, the role of vmiRs in pulpal disease is yet to be explored. The purpose of this study was to examine the expression of vmiRs in normal and diseased pulps and to identify potential target genes.
METHODS: Total RNA was extracted and quantified from normal and inflamed human pulps (N = 28). Expression profiles of vmiRs were then interrogated using miRNA microarrays (V3) and the miRNA Complete Labeling and Hyb Kit (Agilent Technologies, Santa Clara, CA). To identify vmiRs that were differentially expressed, we applied a permutation test.
RESULTS: Of the 12 vmiRs detected in the pulp, 4 vmiRs (including those from herpesvirus and human cytomegalovirus) were differentially expressed in inflamed pulp compared with normal pulp (P < .05). Using bioinformatics, we identified potential target genes for the differentially expressed vmiRs. They included key mediators involved in the detection of microbial ligands, chemotaxis, proteolysis, cytokines, and signal transduction molecules.
CONCLUSIONS: These data suggest that miRs may play a role in interspecies regulation of pulpal health and disease. Further research is needed to elucidate the mechanisms by which vmiRs can potentially modulate the host response in pulpal disease.
Copyright © 2016 American Association of Endodontists. Published by Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Dental pulp; human; inflammation; microRNA; viral

Mesh:

Substances:

Year:  2016        PMID: 27939730      PMCID: PMC5225660          DOI: 10.1016/j.joen.2016.10.006

Source DB:  PubMed          Journal:  J Endod        ISSN: 0099-2399            Impact factor:   4.171


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