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. 2017 Jan 31;11:7. doi: 10.3389/fncel.2017.00007

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Copyright © 2017 Jiang, Wang, Li, Ma and Wang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Scheme summarizing the results. Microglia activation by prolonged exposure of Aβ induced the accumulation of ROS and decreased SIRT3, MnSOD expression in NSCs, accompanied by cell cycle arrest, increased cell apoptosis and mPTP opening, and enhanced mitochondrial membrane potential (ΔΨm) depolarization. Furthermore, SIRT3 knockdown in NSCs accelerated the cell injury, whereas SIRT3 overexpression protected NSCs against activated microglia-induced cellular dysfunction through mitochondrial apoptosis pathway, including decreased mPTP opening and cyclophilin D (CypD) expression, inhibition of mitochondrial Cyt C release to cytoplasm, declined Bax/Bcl-2 ratio and caspase-3/9 enzymatic activity.