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Differential expression of mRNA and miRNA in guinea pigs following infection with HSV2v.

Abstract
MicroRNAs (miRNAs) are 22-nucleotide single-stranded RNAs which regulate gene expression by targeting 3' untranslated regions. Previous studies have suggested that miRNAs may be used as markers for investigating the molecular regulation of gene expression. In the present study, miRNA and mRNA expression profiles were investigated using a massively parallel next generation sequencing technique to compare herpes simplex virus (HSV)2-infected (n=3) and healthy (n=3) epithelial tissues from guinea pigs. Total RNA was isolated and RNA sequencing was performed using a HiSeq 2000 sequencing system. Differential expression of miRNA and mRNA was analyzed using two-tailed t-tests. A negative correlation was detected between the miRNAs and their predicted target genes. Following infection with HSV2, 205 and 159 miRNAs were demonstrated to be upregulated and downregulated, respectively. These differentially expressed miRNAs were associated with cellular and metabolic processes, biological regulation, response to stimuli and cellular components of the immune system, as determined by functional gene ontology analysis. Following HSV2 infection, 6 upregulated miRNAs including miR-592, miR-1245b-5p, miR-150, miR-342-5p, miR-1245b-3p and miR-124 were demonstrated to participate in the toll-like receptor (TLR) pathway by targeting related genes. These results suggested that the downregulated genes were associated with the TLR pathway after infection with HSV2. The results of reverse transcription-quantitative polymerase chain reaction analysis were consistent with RNA sequencing, indicating that the increased expression of these miRNAs downregulated the TLR pathway-associated genes, which may mediate the progression of HSV2-induced genital herpes.
AuthorsLin Kuang, Yihui Deng, Xiaodan Liu, Zhixiang Zou, Lan Mi
JournalExperimental and therapeutic medicine (Exp Ther Med) Vol. 14 Issue 3 Pg. 2577-2583 (Sep 2017) ISSN: 1792-0981 [Print] Greece
PMID28962197 (Publication Type: Journal Article)

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