Abstract:
:Exosomes derived from Schwann cells have been known to have a variety of functions in the development and repair of the peripheral nervous system, and cyclic AMP (cAMP) is a key inducer of Schwann cell differentiation. In the present study, we aimed to study the effect of exosomes derived from differentiated Schwann cells on the expression of microRNAs (miRNAs). To show that miRNAs were altered from exosomes derived from Schwann cells, we conducted next-generation sequencing (NGS) arrays with exosomes derived from cAMP-induced differentiated Schwann cells and control. NGS arrays revealed that 22 miRNAs, 33 small nucleolar RNAs, one antisense RNA, and two mRNAs were upregulated, while 37 mRNAs, one tRNA, and 35 antisense RNAs were downregulated. We also confirmed that miRNA211 and miR92a-3p were upregulated, while the expression levels of hypoxia-inducible factor, rat cyclin-dependent kinase 2, and rat platelet-derived growth factor C were reduced in exosomes derived from cAMP-induced differentiated Schwann cells. Venn diagrams were used to identify overlapping miRNA targets from highly expressed miRNAs (miR211-5p, miR211-3p, and miR92a-3p). The pathways identified via Kyoto Encyclopedia of Genes and Genomes analysis of the target genes are associated with nerve regeneration and Schwann cell proliferation such as the tumor necrosis factor signaling pathway, dopaminergic synapse, and neurotrophin signaling, and cAMP-dependent signaling pathways. Additionally, we observed that exosomes derived from differentiated Schwann cells suppressed Schwann cell migration, while control exosomes obtained from undifferentiated Schwann cells did not. Together, the results suggested that exosomes released from differentiated Schwann cells regulated Schwann cell migration through changes in miRNA expression.
journal_name
Neuroreportjournal_title
Neuroreportauthors
Sohn EJ,Park HT,Shin YKdoi
10.1097/WNR.0000000000001435subject
Has Abstractpub_date
2020-05-07 00:00:00pages
515-522issue
7eissn
0959-4965issn
1473-558Xpii
00001756-202005010-00002journal_volume
31pub_type
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