Abstract
Neural stem cell (NSC) quiescence plays pivotal roles in avoiding exhaustion of NSCs and securing sustainable neurogenesis in the adult brain. The maintenance of quiescence and transition between proliferation and quiescence are complex processes associated with multiple niche signals and environmental stimuli. Exosomes are small extracellular vesicles (sEVs) containing functional cargos such as proteins, microRNAs, and mRNAs. The role of sEVs in NSC quiescence has not been fully investigated. Here, we applied proteomics to analyze the protein cargos of sEVs derived from proliferating, quiescent, and reactivating NSCs. Our findings revealed fluctuation of expression levels and functional clusters of gene ontology annotations of differentially expressed proteins especially in protein translation and vesicular transport among three sources of exosomes. Moreover, the use of exosome inhibitors revealed exosome contribution to entrance into as well as maintenance of quiescence. Exosome inhibition delayed entrance into quiescence, induced quiescent NSCs to exit from the G0 phase of the cell cycle, and significantly upregulated protein translation in quiescent NSCs. Our results suggest that NSC exosomes are involved in attenuating protein synthesis and thereby regulating the quiescence of NSCs.
Highlights
Neural stem cell (NSC), which are derived from the neuroepithelium of the neural tube, maintain the ability to selfrenew and to give rise to neurons, astrocytes, and oligodendrocytes throughout a whole life
Purifications of Exosomes Secreted From aNSCs, Quiescent NSCs (qNSCs) and reactivating NSCs (reNSCs)
We investigated the roles of small extracellular vesicles (sEVs) secreted from NSCs in quiescent and proliferating conditions using cultured NSCs
Summary
NSCs, which are derived from the neuroepithelium of the neural tube, maintain the ability to selfrenew and to give rise to neurons, astrocytes, and oligodendrocytes throughout a whole life. Quiescent NSCs (qNSCs) rest at the G0 phase of the cell cycle and do not express proliferation markers, such as Ki-67 and MCM2 (Codega et al, 2014). They can be reactivated and re-enter the cell cycle upon proper signals. NSCs maintain a delicate balance with proliferating and quiescence. This equilibrium is essential for NSC homeostasis, and its disruption may lead to brain aging and its associated diseases (Cavallucci et al, 2016). Discrete NSC niche stimuli play indispensable roles in determining whether
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