期刊
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
卷 39, 期 9, 页码 1836-1848出版社
SAGE PUBLICATIONS INC
DOI: 10.1177/0271678X18769770
关键词
AAA plus ATPase; ATAD1; neuroprotection; preconditioning; stroke
资金
- NIH [DA000266, R01 NS067525, R37 NS067525, RO1AG029368]
- American Heart Association [0725470U, 11GRNT7810020, 12SDG8940000]
- Simons Foundation Autism Research Initiative (SFARI)
- National Natural Science Foundation of China [81271415, 31471016]
- National Key Research and Development Program of China [2016YFA0101001]
- CAMS Initiative for Innovative Medicine [2016-I2M-1-008]
Neuronal preconditioning in vitro or in vivo with a stressful but non-lethal stimulus leads to new protein expression that mediates a profound neuroprotection against glutamate excitotoxicity and experimental stroke. The proteins that mediate neuroprotection are relatively unknown and under discovery. Here we find that the expression of the AAA + ATPase Thorase is induced by preconditioning stimulation both in vitro and in vivo. Thorase provides neuroprotection in an ATP-dependent manner against oxygen-glucose deprivation (OGD) neurotoxicity or glutamate N-Methyl-D-aspartate (NMDA) receptor-mediated excitotoxicity in vitro. Knock-down of Thorase prevents the establishment of preconditioning induced neuroprotection against OGD or NMDA neurotoxicity. Transgenic overexpression of Thorase provides neuroprotection in vivo against middle cerebral artery occlusion (MCAO)-induced stroke in mice, while genetic deletion of Thorase results in increased injury in vivo following stroke. These results define Thorase as a neuroprotective protein and understanding Thorase signaling could offer a new therapeutic strategy for the treatment of neurologic disorders.
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