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Preservation of neuronal functions by exosomes derived from different human neural cell types under ischemic conditions
Author(s) -
Deng Mingyang,
Xiao Han,
Peng Hongling,
Yuan Huan,
Xu Yunxiao,
Zhang Guangsen,
Tang Jianguang,
Hu Zhiping
Publication year - 2018
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.13784
Subject(s) - embryonic stem cell , neural stem cell , microvesicles , biology , stem cell , microbiology and biotechnology , progenitor cell , exosome , pi3k/akt/mtor pathway , programmed cell death , neuron , neuroscience , apoptosis , stem cell therapy , neuroprotection , signal transduction , microrna , biochemistry , gene
Stem cell‐based therapies have been reported in protecting cerebral infarction‐induced neuronal dysfunction and death. However, most studies used rat/mouse neuron as model cell when treated with stem cell or exosomes. Whether these findings can be translated from rodent to humans has been in doubt. Here, we used human embryonic stem cell‐derived neurons to detect the protective potential of exosomes against ischemia. Neurons were treated with in vitro oxygen–glucose deprivation ( OGD ) for 1 h. For treatment group, different exosomes were derived from neuron, embryonic stem cell, neural progenitor cell and astrocyte differentiated from H9 human embryonic stem cell and added to culture medium 30 min after OGD (100 μg/mL). Western blotting was performed 12 h after OGD , while cell counting and electrophysiological recording were performed 48 h after OGD . We found that these exosomes attenuated OGD ‐induced neuronal death, Mammalian target of rapamycin ( mTOR ), pro‐inflammatory and apoptotic signaling pathway changes, as well as basal spontaneous synaptic transmission inhibition in varying degrees. The results implicate the protective effect of exosomes on OGD ‐induced neuronal death and dysfunction in human embryonic stem cell‐derived neurons, potentially through their modulation on mTOR , pro‐inflammatory and apoptotic signaling pathways.