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神经元衍生的细胞外囊泡含有突触蛋白，促进树突棘形成，激活TrkB介导的信号传导并维持神经元的复杂性。

Neuron-derived extracellular vesicles contain synaptic proteins, promote spine formation, activate TrkB-mediated signalling and preserve neuronal complexity.

作者信息

Solana-Balaguer Julia, Campoy-Campos Genís, Martín-Flores Núria, Pérez-Sisqués Leticia, Sitjà-Roqueta Laia, Kucukerden Melike, Gámez-Valero Ana, Coll-Manzano Albert, Martí Eulàlia, Pérez-Navarro Esther, Alberch Jordi, Soriano Jordi, Masana Mercè, Malagelada Cristina

机构信息

Departament de Biomedicina, Institut de Neurociències (UBneuro), Universitat de Barcelona, Barcelona, Spain.

Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain.

出版信息

J Extracell Vesicles. 2023 Sep;12(9):e12355. doi: 10.1002/jev2.12355.

DOI:10.1002/jev2.12355
PMID:37743539
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10518375/
Abstract

Extracellular vesicles (EVs) play an important role in intercellular communication as carriers of signalling molecules such as bioactive miRNAs, proteins and lipids. EVs are key players in the functioning of the central nervous system (CNS) by influencing synaptic events and modulating recipient neurons. However, the specific role of neuron-to-neuron communication via EVs is still not well understood. Here, we provide evidence that primary neurons uptake neuron-derived EVs in the soma, dendrites, and even in the dendritic spines, and carry synaptic proteins. Neuron-derived EVs increased spine density and promoted the phosphorylation of Akt and ribosomal protein S6 (RPS6), via TrkB-signalling, without impairing the neuronal network activity. Strikingly, EVs exerted a trophic effect on challenged nutrient-deprived neurons. Altogether, our results place EVs in the spotlight for synaptic plasticity modulation as well as a possible therapeutic tool to fight neurodegeneration.

摘要

细胞外囊泡（EVs）作为生物活性微小RNA、蛋白质和脂质等信号分子的载体，在细胞间通讯中发挥着重要作用。EVs通过影响突触事件和调节受体神经元，在中枢神经系统（CNS）的功能中起着关键作用。然而，通过EVs进行的神经元间通讯的具体作用仍未得到充分理解。在这里，我们提供证据表明，原代神经元在胞体、树突甚至树突棘中摄取神经元衍生的EVs，并携带突触蛋白。神经元衍生的EVs通过TrkB信号通路增加了棘密度，并促进了Akt和核糖体蛋白S6（RPS6）的磷酸化，而不损害神经网络活动。令人惊讶的是，EVs对受到营养剥夺挑战的神经元发挥了营养作用。总之，我们的结果使EVs成为突触可塑性调节以及对抗神经退行性变的一种可能治疗工具的焦点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d884/10518375/2888212dc2ef/JEV2-12-12355-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d884/10518375/f782d99d8040/JEV2-12-12355-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d884/10518375/0bab4c3e2b08/JEV2-12-12355-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d884/10518375/9225bad05978/JEV2-12-12355-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d884/10518375/555c97ea5ce5/JEV2-12-12355-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d884/10518375/2888212dc2ef/JEV2-12-12355-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d884/10518375/f782d99d8040/JEV2-12-12355-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d884/10518375/0bab4c3e2b08/JEV2-12-12355-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d884/10518375/9225bad05978/JEV2-12-12355-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d884/10518375/555c97ea5ce5/JEV2-12-12355-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d884/10518375/2888212dc2ef/JEV2-12-12355-g003.jpg

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