Damage to sensory neurons induces neural repair, regrowth and hyperexcitability. The regulation of such responses to injury must be organized in some way by the neurons. Regulation can occur at the post-transcriptional level via microRNAs (miRNAs). miRNAs are small non-coding RNAs that influence the stability or translation of mRNAs and thereby regulate gene expression. Although nociceptive neurons show transcriptional and post-transcriptional regulatory mechanisms at many levels, miRNAs have not yet been systematically investigated in these neurons. Based on our preliminary array data we investigated the presence of miR-1 in dorsal root ganglion (DRG) neurons of mice and humans. We detected miR-1 in total RNA from human and mouse DRG and localised miR-1 in human and murine sensory neurons in situ. In Situ Hybridization detected miR-1 expression by nearly all DRG neurons. In vitro studies of enriched sensory neuron subpopulations from mouse DRG showed higher miR-1 expression levels in I-B4 negative neurons compared with I-B4 positive cells. Culturing of primary sensory neurons reduced the relative miR-1 expression levels independent of the presence or absence of laminin on the culture substrate. Transfection with a miR-1 mimic induced a massive increase in neuronal miR-1 associated with attenuated neurite outgrowth. This first description of miR-1 in sensory neurons including nociceptors suggests that miR-1 has a role in modulating neurite outgrowth.
|Number of pages||9|
|Journal||Histochemistry and Cell Biology|
|Publication status||Published - Jan 2011|
- In Situ Hybridization