Abstract
BackgroundMicroRNAs (miRs) are an abundant class of small non-coding RNAs (~22 nt) that reprogram gene expression by targeting mRNA degradation and translational disruption. An emerging concept implicates miR coupling with transcription factors in myeloid cell development and function, thus contributing to host defense and inflammation. The important role that these molecules play in the pathogenesis of HIV-1 is only now emerging.ResultsWe provide evidence that exposure of monocyte-derived dendritic cells (MDDCs) to recombinant HIV-1 R5 gp120, but not to CCR5 natural ligand CCL4, influences the expression of a panel of miRs (i.e., miR-21, miR-155 and miR-181b) regulated by STAT3 and potentially targeting genes belonging to the STAT3 signaling pathway. The blockage of gp120-induced STAT3 activation impairs gp120 capacity to modulate the expression level of above mentioned miRs. Predictive analysis of miR putative targets emphasizes that these miRs share common target genes. Furthermore, gene ontology and pathway enrichment analysis outline that these genes mainly belong to biological processes related to regulation of transcription, in a complex network of interactions involving pathways relevant to HIV-DC interaction.ConclusionsOverall, these results point to gp120-triggered modulation of miR expression via STAT3 activation as a novel molecular mechanism exploited by HIV-1 to affect DC biology and thus modulate the immune response through complex regulatory loops involving, at the same time, miRs and transcription factors.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-015-1673-3) contains supplementary material, which is available to authorized users.
Highlights
MicroRNAs are an abundant class of small non-coding RNAs (~22 nt) that reprogram gene expression by targeting mRNA degradation and translational disruption
We have recently reported that exposure of monocyte-derived dendritic cells (MDDCs) to
The new data provided by the present study add further complexity to the model we previously postulated to describe the interaction between Dendritic cells (DCs) and HIV-1 in the absence of productive infection
Summary
MicroRNAs (miRs) are an abundant class of small non-coding RNAs (~22 nt) that reprogram gene expression by targeting mRNA degradation and translational disruption. MicroRNAs (miRs) are an abundant class of small noncoding RNAs (~22 nt) that function to control gene expression and restrict viral replication in host cells [1, 2]. Growing evidence indicates that miRs and transcription factors can jointly regulate target gene expression in the form of feedforward or feedback loops [3]. Several cellular miRs show substantial changes in expression upon HIV-1 infection [6, 7], and contributes to viral latency in primary CD4+ T lymphocytes [8]. Changes in miRs expression profile of CD4+ T lymphocytes after exposure to HIV-1 allowed to discriminate among different stages of HIV infection [10]
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