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Nicotinamide Mononucleotide Adenylyltransferase 2 maintains neuronal structural integrity through the maintenance of golgi structure
Neurochemistry international ( IF 4.2 ) Pub Date : 2018-09-29 , DOI: 10.1016/j.neuint.2018.09.010
Tana Pottorf , Alexis Mann , Shaneann Fross , Clayton Mansel , Bhupinder P.S. Vohra

Golgi fragmentation and loss of Nicotinamide Mononucleotide Adenylyltransferase 2 (NMNAT2) are the early key features of many neurodegenerative disorders. We investigated the link between NMNAT2 loss, Golgi fragmentation and axon degeneration. Golgi fragmentation in the cultured dorsal root ganglion (DRG) neurons resulted in caspase dependent axon degeneration and neuronal cell death. NMNAT2 depletion in the DRG neurons caused Golgi fragmentation and caspase dependent axon degeneration. NMNAT2 depletion did not cause ATP loss in the axons. These results indicate that NMNAT2 is required for maintenance of Golgi structure. Loss of Golgi structure or Nmnat2 depletion causes caspase dependent neurodegeneration. cytNmnat1 overexpression inhibited the axon degeneration induced by Golgi fragmentation or NMNAT2 depletion. These results also suggest that these degeneration signals converge on a common cytNmnat1 mediated axon protective program and are distinct from the SARM1 mediated caspase independent axon degeneration.



中文翻译:

烟酰胺单核苷酸腺苷酸转移酶2通过维持高尔基体结构来维持神经元结构完整性

高尔基体的分裂和烟酰胺单核苷酸腺苷酸转移酶2(NMNAT2)的丢失是许多神经退行性疾病的早期关键特征。我们调查了NMNAT2丢失,高尔基体碎裂和轴突变性之间的联系。培养的背根神经节(DRG)神经元中的高尔基体碎裂导致caspase依赖性轴突变性和神经元细胞死亡。DRG神经元中的NMNAT2耗竭导致高尔基体碎裂和caspase依赖性轴突变性。NMNAT2耗竭不会导致轴突中的ATP损失。这些结果表明,NMNAT2是维持高尔基体结构所必需的。高尔基体结构丢失或Nmnat2耗竭会导致caspase依赖性神经变性。cytNmnat1的过表达抑制了高尔基体片段化或NMNAT2耗尽引起的轴突变性。

更新日期:2018-09-29
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