Abstract:
:LPS-induced microglial activation has a major influence on neuronal damage in the inflammatory process. Integral to this is the cellular and molecular interaction between microglia and neurons. Exosomes, a mediator of communication between cells, can transfer lipids, proteins and nucleic acids, affecting many donor and recipient cells. To investigate the mechanism by which microglial exosomes regulate neuronal inflammation after traumatic brain injury, this study primarily analyzed the effect of microglial exosomes on neuronal apoptosis. Exosomes derived from lipopolysaccharide (LPS)-activated microglial cultures were identified and purified. Neurons treated with these exosomes underwent apoptosis. A20 (also known as TNF-inducible protein 3, TNFAIP3) is a deubiquitinating enzyme with key anti-inflammatory functions. A20 is of huge significance to the degeneration and development of neuron. Importantly, A20 protects the exosomes-induced neuronal death, while A20 knockdown increases neuronal death. This study shows that exosomes may be critical for communication between microglia and neurons.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Chen X,Qian B,Kong X,Hao J,Ye Y,Yang K,Xu T,Zhang Fdoi
10.1016/j.neulet.2019.134480subject
Has Abstractpub_date
2019-11-01 00:00:00pages
134480eissn
0304-3940issn
1872-7972pii
S0304-3940(19)30583-Xjournal_volume
712pub_type
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
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