Activity-associated miRNA are packaged in Map1b-enriched exosomes released from depolarized neurons.
Activity-associated miRNA are packaged in Map1b-enriched exosomes released from depolarized neurons.
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DOI：
10.1093/nar/gku594
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发表时间：
2014-08
影响因子：
14.9
通讯作者：
Cairns MJ
中科院分区：
文献类型：
--
作者：
Goldie BJ;Dun MD;Lin M;Smith ND;Verrills NM;Dayas CV;Cairns MJ
基因表达的快速输入限制性变化是突触可塑性的一个重要方面，需要复杂的转录后mRNA运输和调节机制。小的非编码miRNA通过为通用序列依赖性RNA结合复合物提供基于核酸的特异性组分而独特地准备支持这些功能。我们研究了这些分子在静息状态和氯化钾去极化的人神经母细胞中的亚细胞分布，发现在神经突中有选择性的富集和耗竭。去极化与miRNA表达的神经突限制性减少相关;这些分子的一个子集从核酸酶抗性细胞外外泌体的去极化培养基中回收。这些囊泡富含灵长类动物特异性miRNA和突触可塑性相关蛋白MAP 1b。这些发现进一步支持了miRNA作为神经可塑性调节剂的作用，因为它们在神经元中被区室化，并经历活动相关的再分布或释放到细胞外基质中。
Rapid input-restricted change in gene expression is an important aspect of synaptic plasticity requiring complex mechanisms of post-transcriptional mRNA trafficking and regulation. Small non-coding miRNA are uniquely poised to support these functions by providing a nucleic-acid-based specificity component for universal-sequence-dependent RNA binding complexes. We investigated the subcellular distribution of these molecules in resting and potassium chloride depolarized human neuroblasts, and found both selective enrichment and depletion in neurites. Depolarization was associated with a neurite-restricted decrease in miRNA expression; a subset of these molecules was recovered from the depolarization medium in nuclease resistant extracellular exosomes. These vesicles were enriched with primate specific miRNA and the synaptic-plasticity-associated protein MAP1b. These findings further support a role for miRNA as neural plasticity regulators, as they are compartmentalized in neurons and undergo activity-associated redistribution or release into the extracellular matrix.
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影响因子：
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作者：
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通讯作者：
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作者：
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