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Modified Exosomes Reduce Apoptosis and Ameliorate Neural Deficits Induced by Traumatic Brain Injury

Wang, Bo*; Han, Shuangshuang

doi: 10.1097/MAT.0000000000000810
Tissue Engineering/Biomaterials

Apoptosis contributes to the pathogenesis of traumatic brain injury (TBI). Engineered exosomes incorporated with therapeutic nuclear acids have been explored for gene therapy for human diseases. The current study sought to investigate the effect of modified exosome-containing plasmids expressing B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X-protein (Bax) short hairpin RNA (shRNA) on apoptosis and neural functions after TBI. C57BL/6J mice were subjected to controlled cortical impact injury and were treated with the modified exosomes. The results showed that modified exosomes attenuated the decrease of myeloid cell leukemia-1 (Mcl-1), X-linked inhibitor of apoptosis protein (XIAP), and Survivin protein levels in the brain and reduced Cytochrome c release from mitochondria to cytosol after TBI. They also attenuated the impairments of miniature excitatory postsynaptic current (mEPSC) and long-term potentiation (LTP) in the hippocampus of TBI mice and improved the motor and cognitive behaviors after TBI. These results suggested that the modified exosomes might reduce apoptosis and ameliorate neural and functional deficits in mouse models of TBI.

From the *Emergency Department, Cangzhou Central Hospital, Hebei, China

Cangzhou Medical College, Hebei, China.

Submitted for consideration December 2017; accepted for publication in revised form March 2018.

Disclosure: The authors have no conflicts of interest to report.

Conflict of Interest and Source of Funding Statement: None.

Correspondence: Bo Wang, Emergency Department, Cangzhou Central Hospital, 16 Xinhua West Road, Cangzhou 061001, Hebei, China. Email:

Copyright © 2019 by the American Society for Artificial Internal Organs