Differential expression of microRNA-1 in dorsal root ganglion neurons
Differential expression of microRNA-1 in dorsal root ganglion neurons
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DOI：
10.1007/s00418-010-0772-0
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发表时间：
2011-01-01
影响因子：
2.3
通讯作者：
Haberberger, Rainer Viktor
中科院分区：
文献类型：
--
作者：
Bastian, Isabell;Tam, Sunil Tam;Haberberger, Rainer Viktor
感觉神经元的损伤会诱导神经修复、再生和过度兴奋。神经元必须以某种方式组织对损伤的这种反应的调节。调控可以通过microRNA（miRNAs）在转录后水平发生。miRNA是影响mRNA的稳定性或翻译从而调节基因表达的小的非编码RNA。虽然伤害感受神经元在许多水平上表现出转录和转录后调节机制，但miRNAs在这些神经元中尚未得到系统的研究。基于我们的初步阵列数据，我们研究了小鼠和人类背根神经节（DRG）神经元中miR-1的存在。我们检测了人和小鼠DRG的总RNA中的miR-1，并在人和小鼠感觉神经元中原位定位miR-1。原位杂交检测了几乎所有DRG神经元的miR-1表达。对来自小鼠DRG的富集感觉神经元亚群的体外研究显示，与I-B4阳性细胞相比，I-B4阴性神经元中的miR-1表达水平更高。初级感觉神经元的培养降低了miR-1的相对表达水平，而与培养基质上是否存在层粘连蛋白无关。用miR-1模拟物转染诱导神经元miR-1的大量增加，与减弱的神经突生长相关。在感觉神经元包括伤害感受器中的miR-1的首次描述表明miR-1在调节神经突生长中具有作用。
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.