microRNAs Play a role in Nicotine Addiction

Researchers at the University of Virginia recently published research results linking microRNA expression with nicotine addition.  Using a rodent miRNA microarray and rat PC12 cell model, they revealed that nicotine selectively modulates expression of multiple miRNAs, indicating that the miRNA pathway is one of cellular mechanisms involved in gene expression regulated by nicotine.

Nicotine modulates expression of miR-140*, which targets the 3k-untranslated region of dynamin 1 gene (Dnm1)

Department of Psychiatry and Neurobehavioral Sciences, University of Virginia, Charlottesville, VA, USA

Abstract

Nicotine stimulation regulates expression of a diversity of genes, but the underlying mechanisms are largely unknown. MicroRNAs (miRNAs) are short endogenous RNAs known to post-transcriptionally regulate gene expression. To test our hypothesis that miRNAs could mediate nicotine’s effect on gene expression regulation, we profiled miRNA expression to explore to what extent miRNAs are modulated by nicotine. Using a rodent miRNA microarray and rat PC12 cell model, we revealed that nicotine selectively modulates expression of multiple miRNAs, indicating that the miRNA pathway is one of cellular mechanisms involved in gene expression regulated by nicotine. Specifically, we demonstrated that nicotine increases expression of miR-140*, coordinated with the nicotine-augmented expression of its hostone WWP2. Further, we demonstrated that miR-140* targets the 3k-untranslated region of dynamin 1 gene (Dnm1), by direct base-pairing. This targeting represses gene translation in the luciferase reporter assay and induces messenger RNA degradation in Dnm1 expression analysis. Consequently, our data indicate that nicotine regulates Dnm1 expression via the miRNA pathway. Because dynamin 1 has an essential role in synaptic endocytosis in the central nervous system, nicotine-induced miRNA-mediated dynamin 1 expression regulation may illustrate its importance in neural plasticity, which underlies a molecular mechanism of nicotine addiction.

[article]

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