Exosomal cargo including microRNA regulates sensory neuron to macrophage communication after nerve trauma.
Exosomal cargo including microRNA regulates sensory neuron to macrophage communication after nerve trauma.
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DOI：
10.1038/s41467-017-01841-5
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发表时间：
2017-11-24
影响因子：
16.6
通讯作者：
Malcangio M
中科院分区：
文献类型：
--
作者：
Simeoli R;Montague K;Jones HR;Castaldi L;Chambers D;Kelleher JH;Vacca V;Pitcher T;Grist J;Al-Ahdal H;Wong LF;Perretti M;Lai J;Mouritzen P;Heppenstall P;Malcangio M
在外周轴突损伤后，背根神经节（DRG）感觉神经元中发生非编码microRNA（miR）的失调。在这里，我们表明，DRG神经元细胞体释放细胞外囊泡，包括含有miR的外泌体，活动。我们证明了在辣椒素激活TRPV 1受体后，miR-21- 5 p在培养的DRG的外泌体部分中释放。由辣椒素释放的纯感觉神经元衍生的外泌体容易被巨噬细胞吞噬，其中miR-21- 5 p表达的增加促进促炎表型。在小鼠中神经损伤后，miR-21- 5 p在DRG神经元中上调，并且鞘内递送miR-21- 5 p miR-21和感觉神经元中miR-21的条件性缺失都降低神经性超敏反应以及DRG中炎性巨噬细胞募集的程度。我们认为miR-21的上调和释放有助于周围神经损伤后感觉神经元-巨噬细胞的通讯。已知外来体含有microRNA（miR）。在这里，作者表明背根神经节神经元释放含有miR-21- 5 p的外泌体，这有助于周围神经损伤后的炎性细胞募集。
Following peripheral axon injury, dysregulation of non-coding microRNAs (miRs) occurs in dorsal root ganglia (DRG) sensory neurons. Here we show that DRG neuron cell bodies release extracellular vesicles, including exosomes containing miRs, upon activity. We demonstrate that miR-21-5p is released in the exosomal fraction of cultured DRG following capsaicin activation of TRPV1 receptors. Pure sensory neuron-derived exosomes released by capsaicin are readily phagocytosed by macrophages in which an increase in miR-21-5p expression promotes a pro-inflammatory phenotype. After nerve injury in mice, miR-21-5p is upregulated in DRG neurons and both intrathecal delivery of a miR-21-5p antagomir and conditional deletion of miR-21 in sensory neurons reduce neuropathic hypersensitivity as well as the extent of inflammatory macrophage recruitment in the DRG. We suggest that upregulation and release of miR-21 contribute to sensory neuron–macrophage communication after damage to the peripheral nerve. Exosomes are known to contain microRNAs (miRs). Here the authors show that dorsal root ganglion neurons release exosomes containing miR-21-5p, which contributes to inflammatory cell recruitment following peripheral nerve injury.
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影响因子：
11.1
作者：
Bali, Kiran Kumar;Selvaraj, Deepitha;Satagopam, Venkata P.;Lu, Jianning;Schneider, Reinhard;Kuner, Rohini
通讯作者：
Kuner, Rohini
DOI：
10.1073/pnas.1200448109
发表时间：
2012-03-13
影响因子：
11.1
作者：
Nabhan, Joseph F.;Hu, Ruoxi;Lu, Quan
通讯作者：
Lu, Quan
影响因子：
13.9
作者：
Costigan M;Scholz J;Woolf CJ
通讯作者：
Woolf CJ
影响因子：
8.8
作者：
Park CY;Jeker LT;Carver-Moore K;Oh A;Liu HJ;Cameron R;Richards H;Li Z;Adler D;Yoshinaga Y;Martinez M;Nefadov M;Abbas AK;Weiss A;Lanier LL;de Jong PJ;Bluestone JA;Srivastava D;McManus MT
通讯作者：
McManus MT
影响因子：
4.6
作者：
Headland SE;Jones HR;D'Sa AS;Perretti M;Norling LV
通讯作者：
Norling LV